{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:21:35Z","timestamp":1792131695056,"version":"4.4.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2016,5,24]]},"abstract":"<jats:sec>\n                    <jats:title>Background\u2014<\/jats:title>\n                    <jats:p>Although metabolic reprogramming is critical in the pathogenesis of heart failure, studies to date have focused principally on fatty acid and glucose metabolism. Contribution of amino acid metabolic regulation in the disease remains understudied.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results\u2014<\/jats:title>\n                    <jats:p>Transcriptomic and metabolomic analyses were performed in mouse failing heart induced by pressure overload. Suppression of branched-chain amino acid (BCAA) catabolic gene expression along with concomitant tissue accumulation of branched-chain \u03b1-keto acids was identified as a significant signature of metabolic reprogramming in mouse failing hearts and validated to be shared in human cardiomyopathy hearts. Molecular and genetic evidence identified the transcription factor Kr\u00fcppel-like factor 15 as a key upstream regulator of the BCAA catabolic regulation in the heart. Studies using a genetic mouse model revealed that BCAA catabolic defect promoted heart failure associated with induced oxidative stress and metabolic disturbance in response to mechanical overload. Mechanistically, elevated branched-chain \u03b1-keto acids directly suppressed respiration and induced superoxide production in isolated mitochondria. Finally, pharmacological enhancement of branched-chain \u03b1-keto acid dehydrogenase activity significantly blunted cardiac dysfunction after pressure overload.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>BCAA catabolic defect is a metabolic hallmark of failing heart resulting from Kr\u00fcppel-like factor 15\u2013mediated transcriptional reprogramming. BCAA catabolic defect imposes a previously unappreciated significant contribution to heart failure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.115.020226","type":"journal-article","created":{"date-parts":[[2016,4,9]],"date-time":"2016-04-09T00:04:34Z","timestamp":1460160274000},"page":"2038-2049","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":533,"title":["Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure"],"prefix":"10.1161","volume":"133","author":[{"given":"Haipeng","family":"Sun","sequence":"first","affiliation":[{"name":"From Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China (H.S., M.Z., Y.L., Y.W.); Division of Molecular Medicine, Departments of Anesthesiology, Medicine, and Physiology, Molecular Biology Institute, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California, Los Angeles (H.S., C.G., Z.W., J.-Y.Y., S.R., C.D.R., H.C., X.X., Y.W.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristine C.","family":"Olson","sequence":"additional","affiliation":[{"name":"From Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China (H.S., M.Z., Y.L., Y.W.); Division of Molecular Medicine, Departments of Anesthesiology, Medicine, and Physiology, Molecular Biology Institute, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California, Los Angeles (H.S., C.G., Z.W., J.-Y.Y., S.R., C.D.R., H.C., X.X., Y.W.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Gao","sequence":"additional","affiliation":[{"name":"From Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China (H.S., M.Z., Y.L., Y.W.); Division of Molecular Medicine, Departments of Anesthesiology, Medicine, and Physiology, Molecular Biology Institute, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California, Los Angeles (H.S., C.G., Z.W., J.-Y.Y., S.R., C.D.R., H.C., X.X., Y.W.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Domenick A.","family":"Prosdocimo","sequence":"additional","affiliation":[{"name":"From Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China (H.S., M.Z., Y.L., Y.W.); 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