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2. Heterogenous impairment of α cell function in type 2 diabetes is linked to cell maturation state

Author

Dai, Xiao-Qing, Camunas-Soler, Joan, Briant, Linford J.B., dos Santos, Theodore, Spigelman, Aliya F., Walker, Emily M., Arrojo e Drigo, Rafael, Bautista, Austin, Jones, Robert C., Avrahami, Dana, Lyon, James, Nie, Aifang, Smith, Nancy, Zhang, Yongneng, Johnson, Janyne, Manning Fox, Jocelyn E., Michelakis, Evangelos D., Light, Peter E., Kaestner, Klaus H., Kim, Seung K., Rorsman, Patrik, Stein, Roland W., Quake, Stephen R., and MacDonald, Patrick E.

Published
2022
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3. Assessment of Right Ventricular Function in the Research Setting: Knowledge Gaps and Pathways Forward. An Official American Thoracic Society Research Statement

Author

Lahm, Tim, Douglas, Ivor S, Archer, Stephen L, Bogaard, Harm J, Chesler, Naomi C, Haddad, Francois, Hemnes, Anna R, Kawut, Steven M, Kline, Jeffrey A, Kolb, Todd M, Mathai, Stephen C, Mercier, Olaf, Michelakis, Evangelos D, Naeije, Robert, Tuder, Rubin M, Ventetuolo, Corey E, Vieillard-Baron, Antoine, Voelkel, Norbert F, Vonk-Noordegraaf, Anton, and Hassoun, Paul M

Subjects
Cardiovascular, Heart Disease, Lung, Rare Diseases, Animals, Humans, Research, Societies, Medical, United States, Ventricular Dysfunction, Right, Ventricular Function, Right, right ventricle, pulmonary hypertension, pulmonary embolism, acute respiratory distress syndrome, pulmonary circulation, American Thoracic Society Assembly on Pulmonary Circulation, Medical and Health Sciences, Respiratory System
Abstract

BackgroundRight ventricular (RV) adaptation to acute and chronic pulmonary hypertensive syndromes is a significant determinant of short- and long-term outcomes. Although remarkable progress has been made in the understanding of RV function and failure since the meeting of the NIH Working Group on Cellular and Molecular Mechanisms of Right Heart Failure in 2005, significant gaps remain at many levels in the understanding of cellular and molecular mechanisms of RV responses to pressure and volume overload, in the validation of diagnostic modalities, and in the development of evidence-based therapies.MethodsA multidisciplinary working group of 20 international experts from the American Thoracic Society Assemblies on Pulmonary Circulation and Critical Care, as well as external content experts, reviewed the literature, identified important knowledge gaps, and provided recommendations.ResultsThis document reviews the knowledge in the field of RV failure, identifies and prioritizes the most pertinent research gaps, and provides a prioritized pathway for addressing these preclinical and clinical questions. The group identified knowledge gaps and research opportunities in three major topic areas: 1) optimizing the methodology to assess RV function in acute and chronic conditions in preclinical models, human studies, and clinical trials; 2) analyzing advanced RV hemodynamic parameters at rest and in response to exercise; and 3) deciphering the underlying molecular and pathogenic mechanisms of RV function and failure in diverse pulmonary hypertension syndromes.ConclusionsThis statement provides a roadmap to further advance the state of knowledge, with the ultimate goal of developing RV-targeted therapies for patients with RV failure of any etiology.

Published
2018

6. Dichloroacetate should be considered with platinum-based chemotherapy in hypoxic tumors rather than as a single agent in advanced non-small cell lung cancer

Author

Garon, Edward B, Christofk, Heather R, Hosmer, Wylie, Britten, Carolyn D, Bahng, Agnes, Crabtree, Matthew J, Hong, Candice Sun, Kamranpour, Naeimeh, Pitts, Sharon, Kabbinavar, Fairooz, Patel, Cecil, von Euw, Erika, Black, Alexander, Michelakis, Evangelos D, Dubinett, Steven M, and Slamon, Dennis J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Trials and Supportive Activities, Cancer, Clinical Research, Breast Cancer, Lung Cancer, Lung, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Good Health and Well Being, Administration, Oral, Adult, Aged, Antineoplastic Combined Chemotherapy Protocols, Breast Neoplasms, Carcinoma, Non-Small-Cell Lung, Cell Hypoxia, Cell Line, Tumor, Cell Proliferation, Cisplatin, Dichloroacetic Acid, Docetaxel, Drug Administration Schedule, Female, Humans, Lung Neoplasms, Male, Middle Aged, Oxygen Consumption, Taxoids, Treatment Failure, Dichloroacetate, Non-small cell lung cancer, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

ObjectivesDichloroacetate (DCA) is a highly bioavailable small molecule that inhibits pyruvate dehydrogenase kinase, promoting glucose oxidation and reversing the glycolytic phenotype in preclinical cancer studies. We designed this open-label phase II trial to determine the response rate, safety, and tolerability of oral DCA in patients with metastatic breast cancer and advanced stage non-small cell lung cancer (NSCLC).Materials and methodsThis trial was conducted with DCA 6.25 mg/kg orally twice daily in previously treated stage IIIB/IV NSCLC or stage IV breast cancer. Growth inhibition by DCA was also evaluated in a panel of 54 NSCLC cell lines with and without cytotoxic chemotherapeutics (cisplatin and docetaxel) in normoxic and hypoxic conditions.Results and conclusionsUnder normoxic conditions in vitro, single-agent IC50 was >2 mM for all evaluated cell lines. Synergy with cisplatin was seen in some cell lines under hypoxic conditions. In the clinical trial, after seven patients were enrolled, the study was closed based on safety concerns. The only breast cancer patient had stable disease after 8 weeks, quickly followed by progression in the brain. Two patients withdrew consent within a week of enrollment. Two patients had disease progression prior to the first scheduled scans. Within 1 week of initiating DCA, one patient died suddenly of unknown cause and one experienced a fatal pulmonary embolism. We conclude that patients with previously treated advanced NSCLC did not benefit from oral DCA. In the absence of a larger controlled trial, firm conclusions regarding the association between these adverse events and DCA are unclear. Further development of DCA should be in patients with longer life expectancy, in whom sustained therapeutic levels can be achieved, and potentially in combination with cisplatin.

Published
2014

7. Abstract 13575: Lack of Both Mitochondrial Proteins Sirt3 and Ucp2 in Mice Recapitulates Many Critical Features of Human Pulmonary Arterial Hypertension (PAH), Including Inflammatory Plexogenic Lesions, Supporting the Metabolic Theory of PAH

Author

Zhang, Yongneng, Zervopoulos, Sotirios D, Boukouris, Aristeidis E, Saleme, Bruno, Liu, Yongsheng, Haromy, Alois, Webster, Linda, Tabatabaei Dakhili, Seyed Amirhossein, Ussher, John R, Sutendra, Gopinath, and Michelakis, Evangelos D

Published
2020
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15. A reversible metabolic stress-sensitive regulation of CRMP2A orchestrates EMT/stemness and increases metastatic potential in cancer

Author

Boukouris, Aristeidis E., primary, Zhang, Yongneng, additional, Saleme, Bruno, additional, Kinnaird, Adam, additional, Zhao, Yuan Yuan, additional, Liu, Yongsheng, additional, Zervopoulos, Sotirios D., additional, Das, Subhash K., additional, Mittal, Rohan D., additional, Haromy, Alois, additional, Lorenzana-Carrillo, Maria Areli, additional, Krysler, Amanda R., additional, Cromwell, Christopher R., additional, Hubbard, Basil P., additional, Sutendra, Gopinath, additional, and Michelakis, Evangelos D., additional

Published
2022
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17. SNPs for Genes Encoding the Mitochondrial Proteins Sirtuin3 and Uncoupling Protein 2 Are Associated With Disease Severity, Type 2 Diabetes, and Outcomes in Patients With Pulmonary Arterial Hypertension and This Is Recapitulated in a New Mouse Model Lacking Both Genes

Author

Zhang, Yongneng, primary, Zervopoulos, Sotirios D., additional, Boukouris, Aristeidis E., additional, Lorenzana‐Carrillo, Maria Areli, additional, Saleme, Bruno, additional, Webster, Linda, additional, Liu, Yongsheng, additional, Haromy, Alois, additional, Tabatabaei Dakhili, Seyed Amirhossein, additional, Ussher, John R., additional, Sutendra, Gopinath, additional, and Michelakis, Evangelos D., additional

Published
2021
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19. Abstract 9054: Cell-Specific Regulation of the GATA-4/6 Transcription Factors by the Metabolic Enzyme PKM2 Provides Insight into a Biologic Function Essential for Cardiac Health and Survival

Author

Lorenzana Carrillo, Maria Areli, primary, Gopal, Keshav, additional, Byrne, Nikole J, additional, Saleme, Bruno, additional, Das, Subhash K, additional, Tejay, Saymon, additional, Zhang, Yongneng, additional, Haromy, Alois S, additional, Eaton, Farah, additional, Dyck, Jason R, additional, Michelakis, Evangelos D, additional, and Sutendra, Gopinath, additional

Published
2021
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24. A Mitochondria-K + Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth

Author

Bonnet, Sébastien, Archer, Stephen L., Allalunis-Turner, Joan, Haromy, Alois, Beaulieu, Christian, Thompson, Richard, Lee, Christopher T., Lopaschuk, Gary D., Puttagunta, Lakshmi, Bonnet, Sandra, Harry, Gwyneth, Hashimoto, Kyoko, Porter, Christopher J., Andrade, Miguel A., Thebaud, Bernard, and Michelakis, Evangelos D.

Published
2007
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25. Beneficial Effects of Intermediate Dosage of Anticoagulation Treatment on the Prognosis of Hospitalized COVID-19 Patients: The ETHRA Study

Author

POULAKOU, GARYPHALLIA, primary, DIMAKAKOS, EVANGELOS, additional, KOLLIAS, ANASTASIOS, additional, KYRIAKOULIS, KONSTANTINOS G., additional, RAPTI, VASILIKI, additional, TRONTZAS, IOANNIS, additional, THANOS, CHARALAMPOS, additional, ABDELRASOUL, MAHMOUD, additional, VANTANA, THEODORA, additional, LEONTIS, KONSTANTINOS, additional, KAKALOU, ELENI, additional, ARGYRAKI, KATERINA, additional, BARABOUTIS, IOANNIS, additional, MICHELAKIS, EVANGELOS, additional, GIAMARELLOS-BOURBOULIS, EVANGELOS, additional, DIMAKOU, KATERINA, additional, TSOUKALAS, GEORGIOS, additional, RAPTI, ANGELIKI, additional, MICHELAKIS, EVANGELOS D., additional, and SYRIGOS, KONSTANTINOS N., additional

Published
2021
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27. p53‐Mediated Repression of the PGC1A (PPARG Coactivator 1α) and APLNR (Apelin Receptor) Signaling Pathways Limits Fatty Acid Oxidation Energetics: Implications for Cardio‐oncology

Author

Saleme, Bruno, primary, Das, Subhash K., additional, Zhang, Yongneng, additional, Boukouris, Aristeidis E., additional, Lorenzana Carrillo, Maria Areli, additional, Jovel, Juan, additional, Wagg, Cory S., additional, Lopaschuk, Gary D., additional, Michelakis, Evangelos D., additional, and Sutendra, Gopinath, additional

Published
2020
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29. SNPs for Genes Encoding the Mitochondrial Proteins Sirtuin3 and Uncoupling Protein 2 Are Associated With Disease Severity, Type 2 Diabetes, and Outcomes in Patients With Pulmonary Arterial Hypertension and This Is Recapitulated in a New Mouse Model Lacking Both Genes.

Author

Yongneng Zhang, Zervopoulos, Sotirios D., Boukouris, Aristeidis E., Lorenzana-Carrillo, Maria Areli, Saleme, Bruno, Webster, Linda, Yongsheng Liu, Haromy, Alois, Dakhili, Seyed Amirhossein Tabatabaei, Ussher, John R., Sutendra, Gopinath, Michelakis, Evangelos D., Zhang, Yongneng, Liu, Yongsheng, and Tabatabaei Dakhili, Seyed Amirhossein

Published
2021
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33. Mitochondrial HSP90 Accumulation Promotes Vascular Remodeling in Pulmonary Arterial Hypertension

Author

Boucherat, Olivier, primary, Peterlini, Thibaut, additional, Bourgeois, Alice, additional, Nadeau, Valérie, additional, Breuils-Bonnet, Sandra, additional, Boilet-Molez, Stéphanie, additional, Potus, François, additional, Meloche, Jolyane, additional, Chabot, Sophie, additional, Lambert, Caroline, additional, Tremblay, Eve, additional, Chae, Young Chan, additional, Altieri, Dario C., additional, Sutendra, Gopinath, additional, Michelakis, Evangelos D., additional, Paulin, Roxane, additional, Provencher, Steeve, additional, and Bonnet, Sébastien, additional

Published
2018
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35. Enhancing Insights into Pulmonary Vascular Disease through a Precision Medicine Approach. A Joint NHLBI–Cardiovascular Medical Research and Education Fund Workshop Report

Author

Newman, John H., primary, Rich, Stuart, additional, Abman, Steven H., additional, Alexander, John H., additional, Barnard, John, additional, Beck, Gerald J., additional, Benza, Raymond L., additional, Bull, Todd M., additional, Chan, Stephen Y., additional, Chun, Hyung J., additional, Doogan, Declan, additional, Dupuis, Jocelyn, additional, Erzurum, Serpil C., additional, Frantz, Robert P., additional, Geraci, Mark, additional, Gillies, Hunter, additional, Gladwin, Mark, additional, Gray, Michael P., additional, Hemnes, Anna R., additional, Herbst, Roy S., additional, Hernandez, Adrian F., additional, Hill, Nicholas S., additional, Horn, Evelyn M., additional, Hunter, Kendall, additional, Jing, Zhi-Cheng, additional, Johns, Roger, additional, Kaul, Sanjay, additional, Kawut, Steven M., additional, Lahm, Tim, additional, Leopold, Jane A., additional, Lewis, Greg D., additional, Mathai, Stephen C., additional, McLaughlin, Vallerie V., additional, Michelakis, Evangelos D., additional, Nathan, Steven D., additional, Nichols, William, additional, Page, Grier, additional, Rabinovitch, Marlene, additional, Rich, Jonathan, additional, Rischard, Franz, additional, Rounds, Sharon, additional, Shah, Sanjiv J., additional, Tapson, Victor F., additional, Lowy, Naomi, additional, Stockbridge, Norman, additional, Weinmann, Gail, additional, and Xiao, Lei, additional

Published
2017
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36. Pulmonary Arterial Hypertension

Author

Michelakis, Evangelos D. and Archer, Stephen L.

Subjects
Pulmonary Arterial Hypertension, Pulmonary Artery Smooth Muscle Cell, Primary Pulmonary Hypertension, Pulmonary Arterial Hypertension Patient, humanities, Article, Hereditary Hemorrhagic Telangiectasia
Abstract

The first description of the circulation of blood through the lungs has been attributed to Ibn Nafis (1210–1288).1 The concept was rediscovered by Michael Servetus, a Spanish physician during the Renaissance (1511–1553) and recorded, oddly enough, in two pages of his religious treatise, Christianismi Restitutio (1553).2 The definitive exposition of the pulmonary circulation was made by William Harvey in DeMotu Cordis (1628).3 The first observation of the pulmonary capillaries was first reported by Marcellus Malpighi (1661).4 Heart catheterization in humans, driven by a desire to obtain the perfect mixed venous specimen and measure cardiac output, was first performed in 1929 by the German urologist Forssmann,5 using a ureteral catheter to access his own right atrium. Over a decade later, Cournand and Richards at Columbia University in New York subsequently used right heart catheterization to record pulmonary artery pressure (PAP) in patients with shock and secondary forms of pulmonary hypertension (PHT). For these accomplishments, which were inspired by an interest in the pulmonary circulation and PHT related to mitral stenosis, Forssmann, Cournand, and Richards received the Nobel Prize in 1956.

Published
2007

38. Downregulation of microRNA-126 contributes to the failing right ventricle in pulmonary arterial hypertension

Author

Dahou, Abdellaziz, Charbonneau, Éric, Provencher, Steeve, Thébault, Christophe, Ruffenach, Grégoire, Breuils-Bonnet, Sandra, Bonnet, Sébastien, Johnson, Ian, Perron, Jean, Paulin, Roxane, Tremblay, Ève, Wong, Ryan, Lajoie, Annie C., Joubert, Philippe, Potus, François, Pibarot, Philippe, Michelakis, Evangelos D., Graydon, Colin, Paradis, Renée, Nadeau, Valérie, Dahou, Abdellaziz, Charbonneau, Éric, Provencher, Steeve, Thébault, Christophe, Ruffenach, Grégoire, Breuils-Bonnet, Sandra, Bonnet, Sébastien, Johnson, Ian, Perron, Jean, Paulin, Roxane, Tremblay, Ève, Wong, Ryan, Lajoie, Annie C., Joubert, Philippe, Potus, François, Pibarot, Philippe, Michelakis, Evangelos D., Graydon, Colin, Paradis, Renée, and Nadeau, Valérie

Abstract

Background—Right ventricular (RV) failure is the most important factor of both morbidity and mortality in pulmonary arterial hypertension (PAH). However, the underlying mechanisms resulting in the failed RV in PAH remain unknown. There is growing evidence that angiogenesis and microRNAs are involved in PAH-associated RV failure. We hypothesized that microRNA-126 (miR-126) downregulation decreases microvessel density and promotes the transition from a compensated to a decompensated RV in PAH. Methods and Results—We studied RV free wall tissues from humans with normal RV (n=17), those with compensated RV hypertrophy (n=8), and patients with PAH with decompensated RV failure (n=14). Compared with RV tissues from patients with compensated RV hypertrophy, patients with decompensated RV failure had decreased miR-126 expression (quantitative reverse transcription–polymerase chain reaction; P<0.01) and capillary density (CD31+ immunofluorescence; P<0.001), whereas left ventricular tissues were not affected. miR-126 downregulation was associated with increased Sprouty-related EVH1 domain-containing protein 1 (SPRED-1), leading to decreased activation of RAF (phosphorylated RAF/RAF) and mitogen-activated protein kinase (MAPK); (phosphorylated MAPK/MAPK), thus inhibiting the vascular endothelial growth factor pathway. In vitro, Matrigel assay showed that miR-126 upregulation increased angiogenesis of primary cultured endothelial cells from patients with decompensated RV failure. Furthermore, in vivo miR-126 upregulation (mimic intravenous injection) improved cardiac vascular density and function of monocrotaline-induced PAH animals. Conclusions—RV failure in PAH is associated with a specific molecular signature within the RV, contributing to a decrease in RV vascular density and promoting the progression to RV failure. More importantly, miR-126 upregulation in the RV improves microvessel density and RV function in experimental PAH.

Published
2016

39. Downregulation of microRNA-126 contributes to the failing right ventricle in pulmonary arterial hypertension

Author

Potus, François, Ruffenach, Grégoire, Dahou, Abdellaziz, Thébault, Christophe, Breuils-Bonnet, Sandra, Tremblay, Ève, Nadeau, Valérie, Paradis, Renée, Graydon, Colin, Wong, Ryan, Johnson, Ian, Paulin, Roxane, Lajoie, Annie C., Perron, Jean, Charbonneau, Éric, Joubert, Philippe, Pibarot, Philippe, Michelakis, Evangelos D., Provencher, Steeve, Bonnet, Sébastien, Potus, François, Ruffenach, Grégoire, Dahou, Abdellaziz, Thébault, Christophe, Breuils-Bonnet, Sandra, Tremblay, Ève, Nadeau, Valérie, Paradis, Renée, Graydon, Colin, Wong, Ryan, Johnson, Ian, Paulin, Roxane, Lajoie, Annie C., Perron, Jean, Charbonneau, Éric, Joubert, Philippe, Pibarot, Philippe, Michelakis, Evangelos D., Provencher, Steeve, and Bonnet, Sébastien

Abstract

Background—Right ventricular (RV) failure is the most important factor of both morbidity and mortality in pulmonary arterial hypertension (PAH). However, the underlying mechanisms resulting in the failed RV in PAH remain unknown. There is growing evidence that angiogenesis and microRNAs are involved in PAH-associated RV failure. We hypothesized that microRNA-126 (miR-126) downregulation decreases microvessel density and promotes the transition from a compensated to a decompensated RV in PAH. Methods and Results—We studied RV free wall tissues from humans with normal RV (n=17), those with compensated RV hypertrophy (n=8), and patients with PAH with decompensated RV failure (n=14). Compared with RV tissues from patients with compensated RV hypertrophy, patients with decompensated RV failure had decreased miR-126 expression (quantitative reverse transcription–polymerase chain reaction; P<0.01) and capillary density (CD31+ immunofluorescence; P<0.001), whereas left ventricular tissues were not affected. miR-126 downregulation was associated with increased Sprouty-related EVH1 domain-containing protein 1 (SPRED-1), leading to decreased activation of RAF (phosphorylated RAF/RAF) and mitogen-activated protein kinase (MAPK); (phosphorylated MAPK/MAPK), thus inhibiting the vascular endothelial growth factor pathway. In vitro, Matrigel assay showed that miR-126 upregulation increased angiogenesis of primary cultured endothelial cells from patients with decompensated RV failure. Furthermore, in vivo miR-126 upregulation (mimic intravenous injection) improved cardiac vascular density and function of monocrotaline-induced PAH animals. Conclusions—RV failure in PAH is associated with a specific molecular signature within the RV, contributing to a decrease in RV vascular density and promoting the progression to RV failure. More importantly, miR-126 upregulation in the RV improves microvessel density and RV function in experimental PAH.

Published
2015

40. Mitochondrial HSP90 Accumulation Promotes Vascular Remodeling in Pulmonary Arterial Hypertension.

Author

Boucherat, Olivier, Peterlini, Thibaut, Bourgeois, Alice, Nadeau, Valérie, Breuils-Bonnet, Sandra, Boilet-Molez, Stéphanie, Potus, François, Meloche, Jolyane, Chabot, Sophie, Lambert, Caroline, Tremblay, Eve, Young Chan Chae, Altieri, Dario C., Sutendra, Gopinath, Michelakis, Evangelos D., Paulin, Roxane, Provencher, Steeve, and Bonnet, Sébastien

Subjects
VASCULAR remodeling, PULMONARY hypertension, MOLECULAR chaperones, CELL proliferation, IMMUNOFLUORESCENCE
Abstract

Rationale: Pulmonary arterial hypertension (PAH) is a vascular remodeling disease with a poor prognosis and limited therapeutic options. Although the mechanisms contributing to vascular remodeling in PAH are still unclear, several features, including hyperproliferation and resistance to apoptosis of pulmonary artery smooth muscle cells (PASMCs), have led to the emergence of the cancer-like concept. The molecular chaperone HSP90 (heat shock protein 90) is directly associated with malignant growth and proliferation under stress conditions. In addition to being highly expressed in the cytosol, HSP90 exists in a subcellular pool compartmentalized in the mitochondria (mtHSP90) of tumor cells, but not in normal cells, where it promotes cell survival. Objectives: We hypothesized that mtHSP90 in PAH-PASMCs represents a protective mechanism against stress, promoting their proliferation and resistance to apoptosis. Methods: Expression and localization of HSP90 were analyzed by Western blot, immunofluorescence, and immunogold electron microscopy. In vitro, effects of mtHSP90 inhibition on mitochondrial DNA integrity, bioenergetics, cell proliferation and resistance to apoptosis were assessed. In vivo, the therapeutic potential of Gamitrinib, a mitochondria-targeted HSP90 inhibitor, was tested in fawn-hooded and monocrotaline rats. Measurements and Main Results: We demonstrated that, in response to stress, HSP90 preferentially accumulates in PAHPASMC mitochondria (dual immunostaining, immunoblot, and immunogold electron microscopy) to ensure cell survival by preserving mitochondrial DNA integrity and bioenergetic functions. Whereas cytosolic HSP90 inhibition displays a lack of absolute specificity for PAH-PASMCs, Gamitrinib decreased mitochondrial DNA content and repair capacity and bioenergetic functions, thus repressing PAH-PASMC proliferation (Ki67 labeling) and resistance to apoptosis (Annexin V assay) without affecting control cells. In vivo, Gamitrinib improvesPAHin two experimental rat models (monocrotaline and fawn-hooded rat). Conclusions: Our data show for the first time that accumulation of mtHSP90 is a feature of PAH-PASMCs and a key regulator of mitochondrialhomeostasis contributing to vascular remodeling inPAH. [ABSTRACT FROM AUTHOR]

Published
2018
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43. Downregulation of MicroRNA-126 Contributes to the Failing Right Ventricle in Pulmonary Arterial Hypertension

Author

Potus, François, primary, Ruffenach, Grégoire, additional, Dahou, Abdellaziz, additional, Thebault, Christophe, additional, Breuils-Bonnet, Sandra, additional, Tremblay, Ève, additional, Nadeau, Valérie, additional, Paradis, Renée, additional, Graydon, Colin, additional, Wong, Ryan, additional, Johnson, Ian, additional, Paulin, Roxane, additional, Lajoie, Annie C., additional, Perron, Jean, additional, Charbonneau, Eric, additional, Joubert, Philippe, additional, Pibarot, Philippe, additional, Michelakis, Evangelos D., additional, Provencher, Steeve, additional, and Bonnet, Sébastien, additional

Published
2015
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