Sestrin2 prevents age-related intolerance to ischemia and reperfusion injury by modulating substrate metabolism.
Nanhu Quan,Nanhu Quan,Wanqing Sun,Wanqing Sun,Lin Wang,Lin Wang,Xu Chen,Jonathan S. Bogan,Xinchun Zhou,Courtney Cates,Quan Liu,Yang Zheng,Ji Li +12 more
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TLDR
Sesn2 is a scaffold protein that mediates AMPK activation in the ischemic myocardium via an interaction with AMPK upstream LKB1 that prevents age‐related intolerance to ischemia and reperfusion injury by modulating substrate metabolism.Citations
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mTOR as a central regulator of lifespan and aging.
David Papadopoli,Karine Boulay,Lawrence Kazak,Michael Pollak,Frédérick A. Mallette,Ivan Topisirovic,Laura Hulea +6 more
TL;DR: This review highlights the emerging insights that link mTOR to various processes related to aging, such as nutrient sensing, maintenance of proteostasis, autophagy, mitochondrial dysfunction, cellular senescence, and decline in stem cell function.
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Activation of AMPK inhibits inflammatory response during hypoxia and reoxygenation through modulating JNK-mediated NF-κB pathway.
Xu Chen,Xuan Li,Wenyan Zhang,Jie He,Bo Xu,Bin Lei,Zhenhua Wang,Courtney Cates,Thomas Rousselle,Ji Li +9 more
TL;DR: Cardiac AMPK activation plays a critical role in maintaining mitochondrial function and inhibiting the inflammatory response caused by ischemic insults and modulates JNK-NF-κB signaling cascade during hypoxia and reoxygenation stress conditions.
Journal ArticleDOI
Mitophagy and mitochondrial integrity in cardiac ischemia-reperfusion injury.
TL;DR: This review will revisit the contemporary understanding of mitophagy in the regulation of cardiac homeostasis and update recent progresses with regards toMitophagy and cardiac IR injury to establish a role for Mitophagy as a potential therapeutic target in the management of IR injury.
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Abstract 11766: Sestrin2 Promotes LKB1-Mediated AMPK Activation in the Ischemic Heart
TL;DR: Wang et al. as discussed by the authors found that Sestrin2 protein was found to be expressed in adult cardiomyocytes and accumulated in the heart during ischemic conditions.
Journal ArticleDOI
Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging
TL;DR: The role of mitochondrial homeostasis in the regulation of lifespan and healthspan should offer promising novel therapeutic strategies against aging-related complications, particularly cardiovascular diseases.
References
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Journal ArticleDOI
Myocardial Reperfusion Injury
TL;DR: This review focuses on the mechanisms of the injury, on attempts to protect the heart against it, and on promising new approaches to cardioprotection during percutaneous coronary intervention.
Journal ArticleDOI
The stunned myocardium: prolonged, postischemic ventricular dysfunction.
TL;DR: If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardia perfusion by surgical treatment.
Journal ArticleDOI
Clinical Utility of Doppler Echocardiography and Tissue Doppler Imaging in the Estimation of Left Ventricular Filling Pressures A Comparative Simultaneous Doppler-Catheterization Study
Steve R. Ommen,Rick A. Nishimura,Christopher P. Appleton,Fletcher A. Miller,J K Oh,Margaret M. Redfield,Abdul J. Tajik +6 more
TL;DR: The combination of tissue Doppler imaging of the mitral annulus and mitral inflow velocity curves provides better estimates of LV filling pressures than other methods (pulmonary vein, preload reduction), however, accurate prediction of filling pressures for an individual patient requires a stepwise approach incorporating all available data.
Journal ArticleDOI
p53 Target Genes Sestrin1 and Sestrin2 Connect Genotoxic Stress and mTOR Signaling
Andrei V. Budanov,Michael Karin +1 more
TL;DR: Sestrin1 and Sestrin2 provide an important link between genotoxic stress, p53 and the mTOR signaling pathway and are demonstrated to activate the AMP-responsive protein kinase (AMPK) and target it to phosphorylate TSC2 and stimulate its GAP activity, thereby inhibiting mTOR.
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