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Xiongwen Chen
Researcher at Temple University
Publications - 116
Citations - 7762
Xiongwen Chen is an academic researcher from Temple University. The author has contributed to research in topics: Myocyte & Heart failure. The author has an hindex of 43, co-authored 109 publications receiving 6707 citations. Previous affiliations of Xiongwen Chen include Third Military Medical University & Second Military Medical University.
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Journal ArticleDOI
A peptide encoded by a transcript annotated as long noncoding RNA enhances SERCA activity in muscle
Benjamin R. Nelson,Catherine A. Makarewich,Douglas M. Anderson,Benjamin R. Winders,Constantine D Troupes,Fenfen Wu,Austin L Reese,John R. McAnally,Xiongwen Chen,Ege T. Kavalali,Stephen C. Cannon,Steven R. Houser,Rhonda Bassel-Duby,Eric N. Olson +13 more
TL;DR: Dwarf open reading frame (DWORF) is the only endogenous peptide known to activate the SERCA pump by physical interaction and provides a means for enhancing muscle contractility.
Journal ArticleDOI
Cellular Basis of Abnormal Calcium Transients of Failing Human Ventricular Myocytes
Valentino Piacentino,Christopher R. Weber,Xiongwen Chen,Jutta Weisser-Thomas,Kenneth B. Margulies,Donald M. Bers,Steven R. Houser +6 more
TL;DR: Changes in the respective roles of the L-type Ca2+ current, SR Ca 2+ uptake, storage and release, Ca2+, transport via the Na+-Ca2+ exchanger (NCX), and Ca2- buffering in the altered Ca2 + transients of failing human ventricular myocytes can explain the defective Ca2+.
Journal ArticleDOI
Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure
Hiroyuki Nakayama,Xiongwen Chen,Christopher P. Baines,Raisa Klevitsky,Xiaoying Zhang,Hongyu Zhang,Naser Jaleel,Balvin H.L. Chua,Timothy E. Hewett,Jeffrey Robbins,Steven R. Houser,Jeffery D. Molkentin,Jeffery D. Molkentin +12 more
TL;DR: This paradigm of mitochondrial- and necrosis-dependent heart failure was also observed in other mouse models of disease, which supports the concept that heart failure is a pleiotropic disorder that involves not only apoptosis, but also necrotic loss of myocytes in association with dysregulated Ca2+ handling and beta-adrenergic receptor signaling.
cardiomyocyte necrosis as a primary mediator of heart failure
Journal ArticleDOI
Bone marrow cells adopt the cardiomyogenic fate in vivo
Marcello Rota,Jan Kajstura,Toru Hosoda,Claudia Bearzi,Serena Vitale,Grazia Esposito,Grazia Iaffaldano,M. Elena Padin-Iruegas,Arantxa Gonzalez,Roberto Rizzi,Narissa Small,John A. Muraski,Roberto Alvarez,Xiongwen Chen,Konrad Urbanek,Roberto Bolli,Steven R. Houser,Annarosa Leri,Mark A. Sussman,Piero Anversa +19 more
TL;DR: The results indicate that BMCs engraft, survive, and grow within the spared myocardium after infarction by forming junctional complexes with resident myocytes, and BMCs transdifferentiate and acquire the cardiomyogenic and vascular phenotypes restoring the infarcted heart.