Year: 2019
Type: article
Abstract: Mitochondria have emerged as a central factor in the pathogenesis and progression of heart failure, and other cardiovascular diseases, as well, but no therapies are available to treat mitochondrial dysfunction. The National Heart, Lung, and Blood Institute convened a group of leading experts in heart failure, cardiovascular diseases, and mitochondria research in August 2018. These experts reviewed the current state of science and identified key gaps and opportunities in basic, translational, and clinical research focusing on the potential of mitochondria-based therapeutic strategies in heart failure. The workshop provided short- and long-term recommendations for moving the field toward clinical strategies for the prevention and treatment of heart failure and cardiovascular diseases by using mitochondria-based approaches.
Source: Circulation
Authors: Rong Tian, Wilson S. Colucci, Zoltan Arany, Markus M. Bachschmid, Scott W. Ballinger, Sihem Boudina, James E. Bruce, David W. Busija, Sergey Dikalov, Gerald W. Dorn, Zorina S. Galis, Roberta A. Gottlieb, Daniel P. Kelly, Richard N. Kitsis, Mark J. Kohr, Daniel Levy, E. Douglas Lewandowski, Joseph M. McClung, Daria Mochly-Rosen, Kevin D. O’Brien, Brian O’Rourke, Joon-Young Park, Peipei Ping, Michael N. Sack, Shey-Shing Sheu, Yang Shi, Sruti Shiva, Douglas C. Wallace, Robert G. Weiss, Hilary J. Vernon, Renee Wong, Lisa Schwartz Longacre, Scarlet Shi
Institutions: University of Washington, Boston University, University of Pennsylvania, University of Alabama at Birmingham, University of Utah, Tulane University, Vanderbilt University Medical Center, Washington University in St. Louis, National Institutes of Health, National Heart, Lung, and Blood Institute, Cedars-Sinai Medical Center, Cedars-Sinai Smidt Heart Institute, Albert Einstein College of Medicine, Johns Hopkins University, The Ohio State University, East Carolina University, Stanford University, Temple University, University of California, Los Angeles, Thomas Jefferson University, University of Pittsburgh, Children's Hospital of Philadelphia
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
Funders: U.S. Department of Health and Human Services, American Heart Association, Children's Hospital of Philadelphia, Vanderbilt University, University of Pennsylvania, Ohio State University, University of Washington, Tulane University, Johns Hopkins University, University of Pittsburgh, East Carolina University, Thomas Jefferson University, Temple University, Cedars-Sinai Medical Center, Vanderbilt University Medical Center, National Institutes of Health, University of California, Los Angeles, National Heart, Lung, and Blood Institute, National Institute of Mental Health, National Institute of General Medical Sciences, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Neurological Disorders and Stroke, National Center for Advancing Translational Sciences
Awards: G1078383704, G1081001215, G1272390172, G1316145953, Ca2+ and ROS Crosstalk Signaling in Cardiac Mitochondria, G137686275, G1406667714, G1407283284, G1436336173, G1442900148, G2019558206, G2068232658, Regulation of the Dynamic Proteome after Ischemic Injury, G214092936, G2295279302, G2297372303, G235116316, Oxidative Stress in Myocardial Remodeling and Failure, G2525868669, G2866168081, G2868520150, G2979242678, Probing the Role of Mitochondrial Short-chain Carbon Homeostasis in the Hypertrophied and Failing Heart, G3199061093, G3265275079, G3426757398, Molecular Determinants of Mitochondrial Instability and Arrhythmias, Quantitation of protein interactions in cancer cells, G3791999518, Magnetic Resonance of Cardiac C13 Flux & Metabolism Rate, G4063325221, G425396588, A MITOCHONDRIAL-INTERNEURONAL HYPOTHESIS OF AUTISM, G4705346009, G4726664506, G477853788, Genetic Determinants of Limb Pathology in Peripheral Artery Disease, G5151931745, G5222000999, G533075228, G5402081587, G61989656, G6310176720, G63429406, Mitochondrial Inborn Errors in Metabolism, Mouse models for mitochondrial disorders caused by mutations in mtDNA, NHLBI PROTEOMICS INITIATIVE, G7059858312, Functional implications of fluid shear stress-induced mitochondrial remodeling, Mitochondrial Turnover in the Human Heart, Maladaptive Expression of Metabolic Enzymes and Activity in Heart Failure, Impaired cysteine-thiol redox signaling in metabolic cardiovascular disease
OpenAlex ID: W2975977230