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1. Involvement of Parkin‐mediated mitophagy in the pathogenesis of chronic obstructive pulmonary disease‐related sarcopenia

Author

Ito, Akihiko, Hashimoto, Mitsuo, Tanihata, Jun, Matsubayashi, Sachi, Sasaki, Ryoko, Fujimoto, Shota, Kawamoto, Hironori, Hosaka, Yusuke, Ichikawa, Akihiro, Kadota, Tsukasa, Fujita, Yu, Takekoshi, Daisuke, Ito, Sabro, Minagawa, Shunsuke, Numata, Takanori, Hara, Hiromichi, Matsuoka, Tatsuki, Udaka, Jun, Araya, Jun, Saito, Mitsuru, and Kuwano, Kazuyoshi

Subjects
Chronic Obstructive Pulmonary Disease, Tobacco, Tobacco Smoke and Health, Lung, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Musculoskeletal, Animals, Humans, Mice, Mice, Inbred C57BL, Mitophagy, Muscular Atrophy, Pulmonary Disease, Chronic Obstructive, Reactive Oxygen Species, Sarcopenia, Ubiquitin-Protein Ligases, COPD, Parkin, Muscle atrophy, Cigarette smoke, Muscle contraction, Physiology, Clinical Sciences, Human Movement and Sports Sciences
Abstract

BackgroundSarcopenia is characterized by the loss of skeletal muscle mass and strength and is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) exposure, a major cause for COPD, induces mitochondrial damage, which has been implicated in sarcopenia pathogenesis. The current study sought to examine the involvement of insufficient Parkin-mediated mitophagy, a mitochondrion-selective autophagy, in the mechanisms by which dysfunctional mitochondria accumulate with excessive reactive oxygen species (ROS) production in the development of COPD-related sarcopenia.MethodsThe involvement of Parkin-mediated mitophagy was examined using in vitro models of myotube formation, in vivo CS-exposure model using Parkin-/- mice, and human muscle samples from patients with COPD-related sarcopenia.ResultsCigarette smoke extract (CSE) induced myotube atrophy with concomitant 30% reduction in Parkin expression levels (P

Published
2022

4. PRKN-regulated mitophagy and cellular senescence during COPD pathogenesis

Author

Araya, Jun, Tsubouchi, Kazuya, Sato, Nahoko, Ito, Saburo, Minagawa, Shunsuke, Hara, Hiromichi, Hosaka, Yusuke, Ichikawa, Akihiro, Saito, Nayuta, Kadota, Tsukasa, Yoshida, Masahiro, Fujita, Yu, Utsumi, Hirofumi, Kobayashi, Kenji, Yanagisawa, Haruhiko, Hashimoto, Mitsuo, Wakui, Hiroshi, Ishikawa, Takeo, Numata, Takanori, Kaneko, Yumi, Asano, Hisatoshi, Yamashita, Makoto, Odaka, Makoto, Morikawa, Toshiaki, Nishimura, Stephen L, Nakayama, Katsutoshi, and Kuwano, Kazuyoshi

Subjects
Biochemistry and Cell Biology, Biological Sciences, Lung, Tobacco, Chronic Obstructive Pulmonary Disease, Tobacco Smoke and Health, 2.1 Biological and endogenous factors, Respiratory, Inflammatory and immune system, Animals, Cell Cycle Proteins, Cell Line, Cellular Senescence, Cigarette Smoking, Disease Models, Animal, Epithelial Cells, Humans, Membrane Transport Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Microscopy, Electron, Mitochondria, Mitophagy, Nuclear Proteins, PTEN Phosphohydrolase, Protein Kinases, Pulmonary Disease, Chronic Obstructive, Pyridones, Reactive Oxygen Species, Ubiquitin-Protein Ligases, Cellular senescence, COPD, mitophagy, PINK1, PRKN, Biochemistry & Molecular Biology, Biochemistry and cell biology
Abstract

Cigarette smoke (CS)-induced accumulation of mitochondrial damage has been widely implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Mitophagy plays a crucial role in eliminating damaged mitochondria, and is governed by the PINK1 (PTEN induced putative protein kinase 1)-PRKN (parkin RBR E3 ubiquitin protein ligase) pathway. Although both increased PINK1 and reduced PRKN have been implicated in COPD pathogenesis in association with mitophagy, there are conflicting reports for the role of mitophagy in COPD progression. To clarify the involvement of PRKN-regulated mitophagy in COPD pathogenesis, prkn knockout (KO) mouse models were used. To illuminate how PINK1 and PRKN regulate mitophagy in relation to CS-induced mitochondrial damage and cellular senescence, overexpression and knockdown experiments were performed in airway epithelial cells (AEC). In comparison to wild-type mice, prkn KO mice demonstrated enhanced airway wall thickening with emphysematous changes following CS exposure. AEC in CS-exposed prkn KO mice showed accumulation of damaged mitochondria and increased oxidative modifications accompanied by accelerated cellular senescence. In vitro experiments showed PRKN overexpression was sufficient to induce mitophagy during CSE exposure even in the setting of reduced PINK1 protein levels, resulting in attenuation of mitochondrial ROS production and cellular senescence. Conversely PINK1 overexpression failed to recover impaired mitophagy caused by PRKN knockdown, indicating that PRKN protein levels can be the rate-limiting factor in PINK1-PRKN-mediated mitophagy during CSE exposure. These results suggest that PRKN levels may play a pivotal role in COPD pathogenesis by regulating mitophagy, suggesting that PRKN induction could mitigate the progression of COPD. Abbreviations: AD: Alzheimer disease; AEC: airway epithelial cells; BALF: bronchoalveolar lavage fluid; AKT: AKT serine/threonine kinase; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CDKN1A: cyclin dependent kinase inhibitor 1A; CDKN2A: cyclin dependent kinase inhibitor 2A; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; CSE: CS extract; CXCL1: C-X-C motif chemokine ligand 1; CXCL8: C-X-C motif chemokine ligand 8; HBEC: human bronchial epithelial cells; 4-HNE: 4-hydroxynonenal; IL: interleukin; KO: knockout; LF: lung fibroblasts; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; 8-OHdG: 8-hydroxy-2'-deoxyguanosine; OPTN: optineurin; PRKN: parkin RBR E3 ubiquitin protein ligase; PCD: programmed cell death; PFD: pirfenidone; PIK3C: phosphatidylinositol-4:5-bisphosphate 3-kinase catalytic subunit; PINK1: PTEN induced putative kinase 1; PTEN: phosphatase and tensin homolog; RA: rheumatoid arthritis; ROS: reactive oxygen species; SA-GLB1/β-Gal: senescence-associated-galactosidase, beta 1; SASP: senescence-associated secretory phenotype; SNP: single nucleotide polymorphism; TNF: tumor necrosis factor.

Published
2019

7. Interstitial Pneumonia in Psoriasis

Author

Kawamoto, Hironori, Hara, Hiromichi, Minagawa, Shunsuke, Numata, Takanori, Araya, Jun, Kaneko, Yumi, Umezawa, Yoshinori, Asahina, Akihiko, Nakagawa, Hidemi, and Kuwano, Kazuyoshi

Published
2018
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8. Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease

Author

Fujii, Satoko, Hara, Hiromichi, Araya, Jun, Takasaka, Naoki, Kojima, Jun, Ito, Saburo, Minagawa, Shunsuke, Yumino, Yoko, Ishikawa, Takeo, Numata, Takanori, Kawaishi, Makoto, Hirano, Jun, Odaka, Makoto, Morikawa, Toshiaki, Nishimura, Stephen, Nakayama, Katsutoshi, and Kuwano, Kazuyoshi

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Tobacco, Lung, Chronic Obstructive Pulmonary Disease, Tobacco Smoke and Health, 2.1 Biological and endogenous factors, Respiratory, Good Health and Well Being, autophagy, COPD, p62, senescence, ubiquitin, Oncology and carcinogenesis
Abstract

Tobacco smoke-induced accelerated cell senescence has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cell senescence is accompanied by the accumulation of damaged cellular components suggesting that in COPD, inhibition of autophagy may contribute to cell senescence. Here we look at whether autophagy contributes to cigarette smoke extract (CSE) - induced cell senescence of primary human bronchial epithelial cells (HBEC), and further evaluate p62 and ubiquitinated protein levels in lung homogenates from COPD patients. We demonstrate that CSE transiently induces activation of autophagy in HBEC, followed by accelerated cell senescence and concomitant accumulation of p62 and ubiquitinated proteins. Autophagy inhibition further enhanced accumulations of p62 and ubiquitinated proteins, resulting in increased senescence and senescence-associated secretory phenotype (SASP) with interleukin (IL)-8 secretion. Conversely, autophagy activation by Torin1, a mammalian target of rapamycin (mTOR inhibitor), suppressed accumulations of p62 and ubiquitinated proteins and inhibits cell senescence. Despite increased baseline activity, autophagy induction in response to CSE was significantly decreased in HBEC from COPD patients. Increased accumulations of p62 and ubiquitinated proteins were detected in lung homogenates from COPD patients. Insufficient autophagic clearance of damaged proteins, including ubiquitinated proteins, is involved in accelerated cell senescence in COPD, suggesting a novel protective role for autophagy in the tobacco smoke-induced senescence-associated lung disease, COPD.

Published
2012

9. A novel senotherapeutic approach for COPD via activating autophagy-lysosome axis

Author

Matsubayashi, Sachi, primary, Hosaka, Yusuke, additional, Ito, Saburo, additional, Araya, Jun, additional, Hirano, Yuta, additional, Fujimoto, Shota, additional, Kawamoto, Hironori, additional, Watanabe, Naoaki, additional, Kadota, Tsukasa, additional, Fujita, Yu, additional, Takekoshi, Daisuke, additional, Minagawa, Shunsuke, additional, Numata, Takanori, additional, Hara, Hiromichi, additional, and Kuwano, Kazuyoshi, additional

Published
2023
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11. Increased levels of prostaglandin E−major urinary metabolite (PGE-MUM) in chronic fibrosing interstitial pneumonia

Author

Horikiri, Tsugumi, Hara, Hiromichi, Saito, Nayuta, Araya, Jun, Takasaka, Naoki, Utsumi, Hirofumi, Yanagisawa, Haruhiko, Hashimoto, Mitsuo, Yoshii, Yutaka, Wakui, Hiroshi, Minagawa, Shunsuke, Ishikawa, Takeo, Shimizu, Kenichiro, Numata, Takanori, Arihiro, Seiji, Kaneko, Yumi, Nakayama, Katsutoshi, Matsuura, Tomokazu, Matsuura, Masaaki, Fujiwara, Mutsunori, Okayasu, Isao, Ito, Satoru, and Kuwano, Kazuyoshi

Published
2017
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13. Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis

Author

Yoshida, Masahiro, Minagawa, Shunsuke, Araya, Jun, Sakamoto, Taro, Hara, Hiromichi, Tsubouchi, Kazuya, Hosaka, Yusuke, Ichikawa, Akihiro, Saito, Nayuta, Kadota, Tsukasa, Sato, Nahoko, Kurita, Yusuke, Kobayashi, Kenji, Ito, Saburo, Utsumi, Hirohumi, Wakui, Hiroshi, Numata, Takanori, Kaneko, Yumi, Mori, Shohei, Asano, Hisatoshi, Yamashita, Makoto, Odaka, Makoto, Morikawa, Toshiaki, Nakayama, Katsutoshi, Iwamoto, Takeo, Imai, Hirotaka, and Kuwano, Kazuyoshi

Published
2019
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15. Risk factors of moderate-to-severe exacerbation in patients with chronic obstructive pulmonary disease (Original)

Author

Numata, Takanori, Araya, Jun, Matsui, Yuma, Okuda, Keitaro, Watanabe, Junko, Takahashi, Naoko, Miyagawa, Hanae, Fujita, Yu, Takekoshi, Daisuke, Utsumi, Hirofumi, Hashimoto, Mitsuo, Ito, Saburo, Wakui, Hiroshi, Minagawa, Shunsuke, Hara, Hiromichi, and Kuwano, Kazuyoshi

Subjects
exacerbation, pneumonia, body mass index, eosinophil, inhaled corticosteroid, chronic obstructive pulmonary disease
Abstract

article

Published
2021

18. Real-World Effectiveness of Dupilumab for Patients with Severe Asthma: A Retrospective Study

Author

Numata,Takanori, Araya,Jun, Miyagawa,Hanae, Okuda,Keitaro, Takekoshi,Daisuke, Hashimoto,Mitsuo, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, Kuwano,Kazuyoshi, Numata,Takanori, Araya,Jun, Miyagawa,Hanae, Okuda,Keitaro, Takekoshi,Daisuke, Hashimoto,Mitsuo, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, and Kuwano,Kazuyoshi

Abstract

Takanori Numata, Jun Araya, Hanae Miyagawa, Keitaro Okuda, Daisuke Takekoshi, Mitsuo Hashimoto, Shunsuke Minagawa, Takeo Ishikawa, Hiromichi Hara, Kazuyoshi Kuwano Department of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, JapanCorrespondence: Takanori Numata, Department of Respiratory Diseases, The Jikei University School of Medicine, 3-25-8 Nishi-Shimbashi, Minato-ku Tokyo, 105-8461, Japan, Tel +81-3-3433-1111 (ext. 3271), Fax +81-3-3433-1020, Email t-numata@Jikei.ac.jpBackground: Treatment with dupilumab, an anti-interleukin (IL)-4 receptor α monoclonal antibody that blocks both the IL-4 and IL-13 pathways, has demonstrated efficacy for the treatment of severe asthma (SA) with type 2 inflammation. However, few studies have focused on the efficacy of this biologic for the treatment of SA in a real-world setting.Methods: From April 2019 to December 2021, 26 Japanese patients with SA received dupilumab at Jikei University Hospital. We retrospectively evaluated the number of moderate-to-severe exacerbations, pulmonary function, maintenance dose of corticosteroids, biomarkers, and adverse events.Results: During a mean follow-up period of 12.6 months, 10 patients received dupilumab as the first biologic, and 16 switched to dupilumab from other biologics. Dupilumab treatment significantly reduced the number of annual exacerbations from 3.4 ± 4.1 to 1.6 ± 2.7 (/person-year, p < 0.01) at the last follow-up regardless of previous biologic use. The Asthma Control Test score significantly improved in all patients by six months after administration but tended to worsen by 24 months in patients with previous biologic use. On the other hand, blood eosinophil counts (BECs) transiently increased and peaked three to six months after administration. The peak timing can be affected by previous biologic use. Adverse events included wheezing immediately after injection, hypereosinophilia, mild conjunctivitis, and relapse of chronic eosinophilic pneumonia

Published
2022

19. Long-Term Efficacy and Clinical Remission After Benralizumab Treatment in Patients with Severe Eosinophilic Asthma: A Retrospective Study

Author

Numata,Takanori, Araya,Jun, Okuda,Keitaro, Miyagawa,Hanae, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, Kuwano,Kazuyoshi, Numata,Takanori, Araya,Jun, Okuda,Keitaro, Miyagawa,Hanae, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, and Kuwano,Kazuyoshi

Abstract

Takanori Numata, Jun Araya, Keitaro Okuda, Hanae Miyagawa, Shunsuke Minagawa, Takeo Ishikawa, Hiromichi Hara, Kazuyoshi Kuwano Division of Respiratory Diseases, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, JapanCorrespondence: Takanori Numata, Email t-numata@jikei.ac.jpBackground: Few studies on the long-term efficacy of benralizumab, an anti-interleukin-5 receptor α monoclonal antibody, have been conducted for patients with severe eosinophilic asthma (SEA), especially regarding the improvement of pulmonary function and clinical remission in a real-world setting.Objective: To elucidate the long-term efficacy and clinical remission rate (CRR) in patients with SEA.Methods: From July 2018 to July 2022, 23 Japanese patients with SEA received benralizumab for two years or more at Jikei University Hospital. We retrospectively evaluated the patients’ characteristics, biomarkers, number of exacerbations, pulmonary function, asthma symptoms, maintenance oral corticosteroid (OCS) dose and CRR.Results: The mean observation period was 38.3 (24– 49) months. Among the 23 patients, 10 patients switched from mepolizumab to benralizumab. After administration of benralizumab, the forced expiratory volume in one second (FEV1) increased and was maintained for two years in the biologic-naïve group and in the switching group (177 ± 404 and 151 ± 236 [mL], respectively, P = 0.80). In all patients, the %FEV1 improved from 76.7 ± 22.9% to 84.3 ± 18.4% (P = 0.016), and the number of annual exacerbations decreased from 2.5 ± 3.3 to 0.74 ± 1.7 (P = 0.014). Furthermore, the Asthma Control Test score significantly improved, and the reduction in OCS dose was maintained for three years. Ultimately, five patients met the clinical remission criteria and exhibited stabilization of pulmonary function, no exacerbation, no OCS use and well-controlled symptoms. The CRR was significantly higher in patients with a blood basophil count (BBC) ≥ 22 than in those w

Published
2022

24. 慢性閉塞性肺疾患(COPD)合併サルコペニア発症へのParkin介在性マイトファジーの関与 (第138回成医会総会一般演題)

Author

Ito, Akihiko, Hashimoto, Mitsuo, Tanihata, Jun, Matsubayashi, Sachi, Sasaki, Ryoko, Fujimoto, Shota, Kawamoto, Hironori, Watanabe, Naoaki, Kadota, Tsukasa, Fujita, Yu, Ito, Saburo, Takekoshi, Daisuke, Minagawa, Shunsuke, Numata, Takanori, Hara, Hiromichi, Matsuoka, Tatsuki, Udaka, Jun, Araya, Jun, Saito, Mitsuru, and Kuwano, Kazuyoshi

Abstract

article

Published
2021

25. Impaired TRIM16-Mediated Lysophagy in Chronic Obstructive Pulmonary Disease Pathogenesis

Author

Araya, Jun, primary, Saito, Nayuta, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Kadota, Tsukasa, additional, Fujita, Yu, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Fujimoto, Shota, additional, Kawamoto, Hironori, additional, Watanabe, Naoaki, additional, Ito, Akihiko, additional, Okuda, Keitaro, additional, Miyagawa, Hanae, additional, Watanabe, Junko, additional, Takekoshi, Daisuke, additional, Utsumi, Hirofumi, additional, Yoshida, Masahiro, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Ito, Saburo, additional, Numata, Takanori, additional, Mori, Shohei, additional, Matsudaira, Hideki, additional, Hirano, Jun, additional, Ohtsuka, Takashi, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2021
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26. Effectiveness of Switching Biologics for Severe Asthma Patients in Japan: A Single-Center Retrospective Study

Author

Numata, Takanori, primary, Araya, Jun, additional, Miyagawa, Hanae, additional, Okuda, Keitaro, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Takekoshi, Daisuke, additional, Hashimoto, Mitsuo, additional, Minagawa, Shunsuke, additional, Ishikawa, Takeo, additional, Hara, Hiromichi, additional, and Kuwano, Kazuyoshi, additional

Published
2021
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27. Effectiveness of Switching Biologics for Severe Asthma Patients in Japan: A Single-Center Retrospective Study

Author

Numata,Takanori, Araya,Jun, Miyagawa,Hanae, Okuda,Keitaro, Fujita,Yu, Utsumi,Hirofumi, Takekoshi,Daisuke, Hashimoto,Mitsuo, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, Kuwano,Kazuyoshi, Numata,Takanori, Araya,Jun, Miyagawa,Hanae, Okuda,Keitaro, Fujita,Yu, Utsumi,Hirofumi, Takekoshi,Daisuke, Hashimoto,Mitsuo, Minagawa,Shunsuke, Ishikawa,Takeo, Hara,Hiromichi, and Kuwano,Kazuyoshi

Abstract

Takanori Numata, Jun Araya, Hanae Miyagawa, Keitaro Okuda, Yu Fujita, Hirofumi Utsumi, Daisuke Takekoshi, Mitsuo Hashimoto, Shunsuke Minagawa, Takeo Ishikawa, Hiromichi Hara, Kazuyoshi Kuwano Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, JapanCorrespondence: Takanori Numata Tel +81-3-3433-1111 (ex 3271)Fax +81-3-3433-1020Email t-numata@jikei.ac.jpBackground: In Japan, biologic therapy was initiated for patients with severe asthma in 2009. In recent years, four biologics with different mechanisms of action have become available in the clinical setting. However, the efficacy of switching between biologics remains uncertain.Methods: To elucidate the efficacy of switching between biologics, 97 patients were enrolled who had received any biologic therapy for severe asthma at Jikei University Hospital, Tokyo, Japan, from July 2009 to December 2020. We retrospectively examined the patient characteristics, biomarkers, pulmonary function test results, selected biologics, and efficacy.Results: Thirty-one males and 66 females received any biologics. The mean age was 53.3 years at the initiation of biologic therapy. Initially, 33, 41, 15 and eight patients received omalizumab, mepolizumab, benralizumab, and dupilumab, respectively. Among three representative indicators for biologics administration, the peripheral blood eosinophil count, serum IgE levels and fractional exhaled nitric oxide, 64% of the patients had two indicators, and 28% had three indicators. Thirty-four patients (35%) switched from the initial biologic to another, and the reasons for switching included persistent asthmatic symptoms (n=22), schedule of hospital visits (n=5), and other reasons. Thus, the treatment was effective in 11 patients after switching. In addition, two patients received combination therapy with different biologics. Eighteen patients (19%) interrupted treatment for various reasons. Regardless of whether the biologic was th

Published
2021

31. Dasatinib-induced Nonspecific Interstitial Pneumonia That Developed 7 Years after the Initiation of Dasatinib

Author

Takekoshi, Daisuke, primary, Matsui, Yuma, additional, Akutsu, Takuya, additional, Nishioka, Ayako, additional, Kiritani, Ayu, additional, Okuda, Keitaro, additional, Watanabe, Junko, additional, Miyagawa, Hanae, additional, Utsumi, Hirohumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Numata, Takanori, additional, Noda, Yuki, additional, Makishima, Rei, additional, Ikegami, Masahiro, additional, Kawabata, Yoshinori, additional, Araya, Jun, additional, and Kuwano, Kazuyoshi, additional

Published
2020
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34. Involvement of Parkin-mediated mitophagy in COPD-related sarcopenia pathogenesis

Author

Ito, Akihiko, primary, Hashimoto, Mitsuo, additional, Tanihata, Jun, additional, Kawamoto, Hironori, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Kadota, Tsukasa, additional, Fujita, Yu, additional, Minagawa, Shunsuke, additional, Numata, Takanori, additional, Hara, Hiromichi, additional, Araya, Jun, additional, and Kuwano, Kazuyoshi, additional

Published
2020
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35. Nrf2-regulated chaperon-mediated autophagy is involved in apoptosis modulation in COPD pathogenesis

Author

Hosaka, Yusuke, primary, Araya, Jun, additional, Fujita, Yu, additional, Tsubouchi, Kazuya, additional, Kadota, Tsukasa, additional, Yoshida, Masahiro, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Kawamoto, Hironori, additional, Watanabe, Naoaki, additional, Ito, Akihiko, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Numata, Takanori, additional, and Kuwano, Kazuyoshi, additional

Published
2020
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36. Chaperone-Mediated Autophagy Suppresses Apoptosis via Regulation of the Unfolded Protein Response during Chronic Obstructive Pulmonary Disease Pathogenesis

Author

Hosaka, Yusuke, primary, Araya, Jun, additional, Fujita, Yu, additional, Kadota, Tsukasa, additional, Tsubouchi, Kazuya, additional, Yoshida, Masahiro, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Kawamoto, Hironori, additional, Watanabe, Naoaki, additional, Ito, Akihiko, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Okuda, Keitaro, additional, Watanabe, Junko, additional, Takekoshi, Daisuke, additional, Utsumi, Hirofumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Ito, Saburo, additional, Numata, Takanori, additional, Mori, Shohei, additional, Matsudaira, Hideki, additional, Hirano, Jun, additional, Ohtsuka, Takashi, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2020
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38. Predictors of the enhanced response to mepolizumab treatment for severe eosinophilic asthma: A retrospective, long-term study

Author

Numata, Takanori, Miyagawa, Hanae, Kawamoto, Hironori, Yoshida, Masahiro, Utsumi, Hirofumi, Hashimoto, Mitsuo, Minagawa, Shunsuke, Hara, Hiromichi, Araya, Jun, and Kuwano, Kazuyoshi

Abstract

Mepolizumab significantly reduces the number of annual exacerbations (AEs) and the maintenance dose of systemic corticosteroids (CSs) in patients with severe eosinophilic asthma (SEA). However, there are few studies based on real life with a long-term observational period in Japan. Between July 2016 and December 2019, 24 Japanese patients received mepolizumab at Jikei University Hospital for at least 12 months. We retrospectively evaluated these characteristics, AEs and CS doses. To elucidate the predictors of the enhanced responders, we performed multivariate logistic regression analysis. After introduction, asthma symptoms improved and were maintained for over a year. The number of AEs and CS doses significantly decreased. In the subgroup analysis, the younger than 65 years-old, body mass index (BMI) < 25 kg/m2, eosinophilic chronic rhinosinusitis, or eosinophil count ≥ 400/mm3 exhibited effective reductions in either AEs or CS doses with mepolizumab treatment. The percentage change in the AEs (≤ −75%) was significantly decreased in the patients with a BMI < 25 using multivariate logistic regression analysis (odds ratio 31, 95% confidence interval: 1.4–700, P = 0.03). In real-life, BMI < 25 could be a predictor for reductions in AEs with mepolizumab treatment in the patients with SEA. IL, interleukin; CS, corticosteroid; SEA, severe eosinophilic asthma; BMI, body mass index; ECRS, eosinophilic chronic rhinosinusitis; CRSwNP, chronic rhinosinusitis with nasal polyps

Published
2020
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40. A case of Aspergillus and Nocardia infections after bronchial thermoplasty

Author

Matsubayashi, Sachi, Iikura, Motoyasu, Numata, Takanori, Izumi, Shinyu, and Sugiyama, Haruhito

Subjects
severe asthma, Aspergillus, bronchial thermoplasty, Case Report, Case Reports, respiratory system, Nocardia, respiratory tract diseases
Abstract

Bronchial thermoplasty (BT) is a bronchoscopic treatment for severe asthma. A 35‐year‐old woman with uncontrolled severe asthma despite maximal pharmacological treatment underwent BT and started coughing after the first procedure. One month later, during the second BT procedure, there were white ulcerous lesions on the right B9 bronchus. Culture of the bronchial brushing specimen showed Aspergillus fumigatus, for which voriconazole was started for treatment. On the third BT procedure, endobronchial mucus sampling demonstrated Nocardia spp., for which trimethoprim‐sulfamethoxazole was given for three months. Seven months after the third BT procedure, no particular endobronchial lesions were found, and no abnormal pathogens were obtained by culture. The resulting bronchial infection in this case may be attributed to the use of systemic steroids, which rendered the patient immunocompromised, and to tissue fragility that was caused by the thermal energy from the BT procedure. Culture of endobronchial mucus should be considered during BT.

Published
2018

41. Involvement of GPx4-Regulated Lipid Peroxidation in Idiopathic Pulmonary Fibrosis Pathogenesis

Author

Tsubouchi, Kazuya, primary, Araya, Jun, additional, Yoshida, Masahiro, additional, Sakamoto, Taro, additional, Koumura, Tomoko, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Kadota, Tsukasa, additional, Kurita, Yusuke, additional, Kobayashi, Kenji, additional, Ito, Saburo, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Mori, Shohei, additional, Asano, Hisatoshi, additional, Matsudaira, Hideki, additional, Ohtsuka, Takashi, additional, Nakayama, Katsutoshi, additional, Nakanishi, Yoichi, additional, Imai, Hirotaka, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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42. Chaperone-mediated autophagy modulates epithelial cell apoptosis in COPD pathogenesis

Author

Hosaka, Yusuke, primary, Araya, Jun, additional, Fujita, Yu, additional, Tsubouchi, Kazuya, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Nakano, Takayuki, additional, Ito, Akihiko, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Kadota, Tsukasa, additional, Yoshida, Masahiro, additional, Hashimoto, Mitsuo, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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43. Lysosomal dysfunction in COPD pathogenesis

Author

Saito, Nayuta, primary, Araya, Jun, additional, Ito, Akihiko, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Kadota, Tsukasa, additional, Nakano, Takayuki, additional, Yoshida, Masahiro, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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44. Role of Parkin in the pathogenesis of COPD-related sarcopenia

Author

Ito, Akihiko, primary, Hashimoto, Mitsuo, additional, Tanihata, Jun, additional, Nakano, Takayuki, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Yoshida, Masahiro, additional, Fujita, Yu, additional, Minagawa, Shunsuke, additional, Numata, Takanori, additional, Hara, Hiromichi, additional, Araya, Jun, additional, Kaneko, Yumi, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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45. Chaperone-Mediated Autophagy-Dependent Chemoresistance in Non-Small Cell Lung Cancer

Author

Ichikawa, Akihiro, primary, Fujita, Yu, additional, Hosaka, Yusuke, additional, Kadota, Tsukasa, additional, Ito, Akihiko, additional, Nakano, Takayuki, additional, Saito, Nayuta, additional, Yoshida, Masahiro, additional, Minagawa, Shunsuke, additional, Numata, Takanori, additional, Hara, Hiromichi, additional, Ochiya, Takahiro, additional, Araya, Jun, additional, Kaneko, Yumi, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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46. Prostaglandin E-Major Urinary Metabolite (PGE-MUM) as a Tumor Marker for Lung Adenocarcinoma

Author

Kawamoto, Hironori, primary, Hara, Hiromichi, additional, Araya, Jun, additional, Ichikawa, Akihiro, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Minagawa, Shunsuke, additional, Numata, Takanori, additional, Arihiro, Seiji, additional, Matsuura, Tomokazu, additional, Fujiwara, Mutsunori, additional, Ito, Satoru, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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47. Involvement of Lamin B1 Reduction in Accelerated Cellular Senescence during Chronic Obstructive Pulmonary Disease Pathogenesis

Author

Saito, Nayuta, primary, Araya, Jun, additional, Ito, Saburo, additional, Tsubouchi, Kazuya, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Ito, Akihiko, additional, Nakano, Takayuki, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Kadota, Tsukasa, additional, Yoshida, Masahiro, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Kurita, Yusuke, additional, Kobayashi, Kenji, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Asano, Hisatoshi, additional, Odaka, Makoto, additional, Ohtsuka, Takashi, additional, Morikawa, Toshiaki, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2019
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48. PRKN-regulated mitophagy and cellular senescence during COPD pathogenesis

Author

Araya, Jun, primary, Tsubouchi, Kazuya, additional, Sato, Nahoko, additional, Ito, Saburo, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Kadota, Tsukasa, additional, Yoshida, Masahiro, additional, Fujita, Yu, additional, Utsumi, Hirofumi, additional, Kobayashi, Kenji, additional, Yanagisawa, Haruhiko, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Ishikawa, Takeo, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Asano, Hisatoshi, additional, Yamashita, Makoto, additional, Odaka, Makoto, additional, Morikawa, Toshiaki, additional, Nishimura, Stephen L, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2018
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49. Dysregulated mitochondrial integrity associated with lamin B1 reduction is involved in cellular senescence progression in COPD pathogenesis

Author

Saito, Nayuta, primary, Araya, Jun, additional, Ito, Saburo, additional, Hosaka, Yusuke, additional, Kadota, Tsukasa, additional, Yoshida, Masahiro, additional, Tsubouchi, Kazuya, additional, Ichikawa, Akihiro, additional, Kurita, Yusuke, additional, Kobayashi, Kenji, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Utsumi, Hirofumi, additional, Yanagisawa, Haruhiko, additional, Hashimoto, Mitsuo, additional, Wakui, Hiroshi, additional, Ishikawa, Takeo, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2018
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50. Involvement of GPx4-regulated lipid peroxidation in IPF pathogenesis.

Author

Tsubouchi, Kazuya, primary, Araya, Jun, additional, Minagawa, Shunsuke, additional, Hara, Hiromichi, additional, Hosaka, Yusuke, additional, Ichikawa, Akihiro, additional, Saito, Nayuta, additional, Yoshida, Masahiro, additional, Ishikawa, Takeo, additional, Numata, Takanori, additional, Kaneko, Yumi, additional, Nakayama, Katsutoshi, additional, and Kuwano, Kazuyoshi, additional

Published
2018
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