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Ming Zheng

Researcher at Peking University

Publications -  89
Citations -  4597

Ming Zheng is an academic researcher from Peking University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 30, co-authored 62 publications receiving 4059 citations. Previous affiliations of Ming Zheng include Chinese Ministry of Education & University of California, San Diego.

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Superoxide Flashes in Single Mitochondria

TL;DR: It is shown that individual mitochondria undergo spontaneous bursts of superoxide generation, termed "superoxide flashes", and proposed that superoxide flashes could serve as a valuable biomarker for a wide variety of oxidative stress-related diseases.
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Dual modulation of cell survival and cell death by beta(2)-adrenergic signaling in adult mouse cardiac myocytes.

TL;DR: In this article, the authors investigate the role of β-adrenergic receptor (AR) and β-AR subtypes in regulating cardiomyocyte survival and apoptosis and explore underlying mechanisms.
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An FHL1-containing complex within the cardiomyocyte sarcomere mediates hypertrophic biomechanical stress responses in mice

TL;DR: Mechanistic studies demonstrated that four-and-a-half LIM domains 1 (FHL1) plays an important role in the mechanism of pathological hypertrophy by sensing biomechanical stress responses via the N2B stretch sensor domain of titin and initiating changes in the titin- and MAPK-mediated responses important for sarcomere extensibility and intracellular signaling.
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p38 Mitogen-Activated Protein Kinase Mediates a Negative Inotropic Effect in Cardiac Myocytes

TL;DR: It is concluded that the negative inotropic effect of p38 MAPK is mediated by decreasing myofilament response to Ca2+, rather than by altering Ca2+i homeostasis and that the reduced my ofilament Ca 2+ sensitivity is unlikely attributable to troponin I phosphorylation or alterations in pHi.
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Central Role of Mitofusin 2 in Autophagosome-Lysosome Fusion in Cardiomyocytes

TL;DR: A novel and essential role of MFN2 is revealed in the cardiac autophagic process by mediating the maturation of autophagy at the phase ofAutophagosome-lysosome fusion, which was markedly retarded without altering the formation of Autophagy and lysosomes in response to ischemia-reperfusion stress.