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7. Role of Sirtuins in Retinal Function Under Basal Conditions

Author

Lin, Jonathan B., Kubota, Shunsuke, Mostoslavsky, Raul, Apte, Rajendra S., COHEN, IRUN R., Series Editor, LAJTHA, ABEL, Series Editor, LAMBRIS, JOHN D., Series Editor, PAOLETTI, RODOLFO, Series Editor, REZAEI, NIMA, Series Editor, Ash, John D., editor, Anderson, Robert E., editor, LaVail, Matthew M., editor, Bowes Rickman, Catherine, editor, Hollyfield, Joe G., editor, and Grimm, Christian, editor

Published
2018
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9. Proliferative Vitreoretinopathy: Pathophysiology and Therapeutic Approaches.

Author

Lin, Jonathan B., Wu, Frances, and Kim, Leo A.

Subjects
*PROLIFERATIVE vitreoretinopathy, *VITRECTOMY, *THERAPEUTICS, *RETINAL surgery, *VASCULAR endothelial growth factor antagonists
Abstract

This article provides an overview of proliferative vitreoretinopathy (PVR), a complication that can occur after retinal detachment surgery. It discusses the classification system for PVR severity and identifies clinical risk factors for its development. The article explores the pathophysiology of PVR, including the breakdown of the blood-retinal barrier and the transformation of retinal pigment epithelial cells. Various therapeutic approaches for PVR are discussed, including corticosteroids, anti-vascular endothelial growth factor agents, and antimetabolites or chemotherapeutics, but none have shown consistent benefits. The article emphasizes the need for further research in this area and provides references for further reading. [Extracted from the article]

Published
2024
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13. Neurofilament Light Chain in Aqueous Humor as a Marker of Neurodegeneration in Glaucoma

Author

Lin,Jonathan B, Pitts,Kristen M, El Helwe,Hani, Neeson,Cameron, Hall,Nathan E, Falah,Henisk, Schultz,Stephanie A, Wang,Silas L, Lo,Kristine, Song,Christian, Margeta,Milica A, Solá-Del Valle,David, Lin,Jonathan B, Pitts,Kristen M, El Helwe,Hani, Neeson,Cameron, Hall,Nathan E, Falah,Henisk, Schultz,Stephanie A, Wang,Silas L, Lo,Kristine, Song,Christian, Margeta,Milica A, and Solá-Del Valle,David

Abstract

Jonathan B Lin,1 Kristen M Pitts,1 Hani El Helwe,1 Cameron Neeson,1 Nathan E Hall,1 Henisk Falah,1 Stephanie A Schultz,2 Silas L Wang,1 Kristine Lo,1 Christian Song,1 Milica A Margeta,1,* David Solá-Del Valle1,* 1Department of Ophthalmology, Harvard Medical School and Massachusetts Eye and Ear, Boston, MA, USA; 2Department of Neurology, Harvard Medical School and Massachusetts General Hospital, Boston, MA, USA*These authors contributed equally to this workCorrespondence: David Solá-Del Valle; Milica A Margeta, Assistant Professor of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, 243 Charles Street, Boston, MA, 02114, USA, Email david_sola-delvalle@meei.harvard.edu; milica_margeta@meei.harvard.eduPurpose: Neurofilament light chain (NfL) is a neuronal cytoskeletal protein that has been identified as a marker of neurodegeneration in diseases of the central nervous system. In this study, we investigated whether NfL in the aqueous humor (AH) can serve as a marker of neurodegeneration in glaucoma in a racially diverse North American population.Design: Single-center, case–control study.Participants: We enrolled patients with various types and stages of glaucoma undergoing planned ophthalmic surgery as part of their routine care and compared them with patients without glaucoma undergoing phacoemulsification for age-related cataract.Methods: We collected AH from 39 glaucoma patients and 10 patients without glaucoma. AH NfL was quantified using the Single-Molecule Array (Simoa)® NF-light assay (Quanterix). Demographic information, such as age, body mass index, sex, and self-reported race, as well as clinical information, such as pre-operative intraocular pressure (IOP), maximum IOP, and number of pre-operative glaucoma medications, was obtained by reviewing the medical record.Main Outcome Measures: Levels of AH NfL.Results: In a model controlling for age and body mass index (BMI), NfL was significantly elevated in AH from glauco

Published
2023

14. Ocular effects of Rho kinase (ROCK) inhibition: a systematic review

Author

Lin, Jonathan B., Harris, James M., Baldwin, George, Goss, Deborah, and Margeta, Milica A.

Abstract

Topical therapies targeting Rho-associated protein kinase (ROCK) signalling, including netarsudil (Rhopressa®) and ripasudil (Glanatec®), have become widely adopted as part of standard clinical practice to lower intraocular pressure (IOP) in patients with ocular hypertension or glaucoma. Given the pleiotropic roles of ROCK signalling, ROCK inhibition has the potential to cause unintended ocular side effects beyond IOP lowering in other substructures of the eye, both beneficial and deleterious. Additional experience and observation of patients treated with this class of medications have uncovered both new side effects not reported in the initial clinical trials, as well as potential benefits that have inspired off-label uses and that have been the topic of numerous clinical studies, case series, case reports, and translational studies. Here, we performed a comprehensive systematic review and identified 170 studies describing ocular effects of ROCK inhibition. In addition to describing well-established ocular effects associated with inhibition of ROCK signalling, such as conjunctival hyperaemia, corneal verticillata, and reticular corneal epithelial oedema, we also highlight other effects, such as corneal haemorrhages, changes in corneal contour, anterior subcapsular opacities, contact dermatitis, punctal stenosis, and eyelid wound dehiscence, which have been described in case series and case reports. Finally, we evaluated studies describing potential novel applications of ROCK inhibition for treating disorders affecting the cornea, the retina, and the optic nerve, finding strong evidence in support of a beneficial effect of ROCK inhibitors on corneal oedema due to corneal endothelial cell dysfunction. The other potential applications require further research.

Published
2024
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30. List of Contributors

Author

Adiga, Shashishekar P., primary, Arenal, Raul, additional, Asmussen, Jes, additional, Auciello, Orlando, additional, Barnard, Amanda S., additional, Butenko, Yuriy V., additional, Chow, Edward K., additional, Curtiss, Larry A., additional, Danilenko, Vycheslav, additional, Gogotsi, Yury, additional, Grotjohn, Timothy A., additional, Gruen, Dieter M., additional, Ho, Dean, additional, Hoffman, Alon, additional, Ivanov, M.G., additional, Ivanov, D.M., additional, Kuznetsov, Vladimir L., additional, Lin, Jonathan B., additional, Man, Han B., additional, Manson, Neil B., additional, Michaelson, Shaul, additional, Mochalin, Vadym, additional, Neitzel, Ioannis, additional, Osawa, Eiji, additional, Robinson, Erik, additional, Sasaki, Shuichi, additional, Schrand, Amanda M., additional, Schuelke, Thomas, additional, Shenderova, Olga A., additional, Shiryaev, Andrey A., additional, Turner, Stuart, additional, Van Tendeloo, Gustaaf, additional, Vlasov, Igor I., additional, Yamanoi, Ryoko, additional, Zapol, Peter, additional, Zhang, Kangyi, additional, and Zvyagin, Andrei V., additional

Published
2012
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37. WNT7A/B promote choroidal neovascularization

Author

Lin, Joseph B., primary, Sene, Abdoulaye, additional, Wiley, Luke A., additional, Santeford, Andrea, additional, Nudleman, Eric, additional, Nakamura, Rei, additional, Lin, Jonathan B., additional, Moolani, Harsh V., additional, and Apte, Rajendra S., additional

Published
2018
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42. GDF15 is elevated in mice following retinal ganglion cell death and in glaucoma patients

Author

Ban, Norimitsu, primary, Siegfried, Carla J., additional, Lin, Jonathan B., additional, Shui, Ying-Bo, additional, Sein, Julia, additional, Pita-Thomas, Wolfgang, additional, Sene, Abdoulaye, additional, Santeford, Andrea, additional, Gordon, Mae, additional, Lamb, Rachel, additional, Dong, Zhenyu, additional, Kelly, Shannon C., additional, Cavalli, Valeria, additional, Yoshino, Jun, additional, and Apte, Rajendra S., additional

Published
2017
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44. NAMPT-Mediated NAD+ Biosynthesis Is Essential for Vision In Mice

Author

Lin, Jonathan B., primary, Kubota, Shunsuke, additional, Ban, Norimitsu, additional, Yoshida, Mitsukuni, additional, Santeford, Andrea, additional, Sene, Abdoulaye, additional, Nakamura, Rei, additional, Zapata, Nicole, additional, Kubota, Miyuki, additional, Tsubota, Kazuo, additional, Yoshino, Jun, additional, Imai, Shin-ichiro, additional, and Apte, Rajendra S., additional

Published
2016
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45. NAD+ and sirtuins in retinal degenerative diseases: A look at future therapies.

Author

Lin, Jonathan B. and Apte, Rajendra S.

Subjects
*SIRTUINS, *DISEASES, *PHENOTYPES, *PHOTORECEPTORS, *DEGENERATION (Pathology)
Abstract

Retinal degenerative diseases are a major cause of morbidity in modern society because visual impairment significantly decreases the quality of life of patients. A significant challenge in treating retinal degenerative diseases is their genetic and phenotypic heterogeneity. However, despite this diversity, many of these diseases share a common endpoint involving death of light-sensitive photoreceptors. Identifying common pathogenic mechanisms that contribute to photoreceptor death in these diverse diseases may lead to a unifying therapy for multiple retinal diseases that would be highly innovative and address a great clinical need. Because the retina and photoreceptors, in particular, have immense metabolic and energetic requirements, many investigators have hypothesized that metabolic dysfunction may be a common link unifying various retinal degenerative diseases. Here, we discuss a new area of research examining the role of NAD+ and sirtuins in regulating retinal metabolism and in the pathogenesis of retinal degenerative diseases. Indeed, the results of numerous studies suggest that NAD+ intermediates or small molecules that modulate sirtuin function could enhance retinal metabolism, reduce photoreceptor death, and improve vision. Although further research is necessary to translate these findings to the bedside, they have strong potential to truly transform the standard of care for patients with retinal degenerative diseases. [ABSTRACT FROM AUTHOR]

Published
2018
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46. NAD+-dependent deacetylase SIRT3 in adipocytes is dispensable for maintaining normal adipose tissue mitochondrial function and whole body metabolism.

Author

Porter, Lane C., Franczyk, Michael P., Pietka, Terri, Yamaguchi, Shintaro, Lin, Jonathan B., Yo Sasaki, Verdin, Eric, Apte, Rajendra S., and Jun Yoshino

Abstract

Mitochondrial dysfunction in adipose tissue is involved in the pathophysiology of obesity-induced systemic metabolic complications, such as type 2 diabetes, insulin resistance, and dyslipidemia. However, the mechanisms responsible for obesity-induced adipose tissue mitochondrial dysfunction are not clear. The aim of present study was to test the hypothesis that nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin-3 (SIRT3) in adipocytes plays a critical role in adipose tissue mitochondrial biology and obesity. We first measured adipose tissue SIRT3 expression in obese and lean mice. Next, adipocyte-specific mitochondrial Sirt3 knockout (AMiSKO) mice were generated and metabolically characterized. We evaluated glucose and lipid metabolism in adult mice fed either a regular-chow diet or high-fat diet (HFD) and in aged mice. We also determined the effects of Sirt3 deletion on adipose tissue metabolism and mitochondrial biology. Supporting our hypothesis, obese mice had decreased SIRT3 gene and protein expression in adipose tissue. However, despite successful knockout of SIRT3, AMiSKO mice had normal glucose and lipid metabolism and did not change metabolic responses to HFD-feeding and aging. In addition, loss of SIRT3 had no major impact on putative SIRT3 targets, key metabolic pathways, and mitochondrial function in white and brown adipose tissue. Collectively, these findings suggest that adipocyte SIRT3 is dispensable for maintaining normal adipose tissue mitochondrial function and whole body metabolism. Contrary to our hypothesis, loss of SIRT3 function in adipocytes is unlikely to contribute to the pathophysiology of obesity-induced metabolic complications. [ABSTRACT FROM AUTHOR]

Published
2018
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