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Nirmala Hariharan

Researcher at University of California, Davis

Publications -  31
Citations -  3857

Nirmala Hariharan is an academic researcher from University of California, Davis. The author has contributed to research in topics: Autophagy & Stem cell. The author has an hindex of 20, co-authored 31 publications receiving 2726 citations. Previous affiliations of Nirmala Hariharan include University of Medicine and Dentistry of New Jersey & Rutgers University.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Deacetylation of FoxO by Sirt1 plays an essential role in mediating starvation-induced autophagy in cardiac myocytes

TL;DR: It is suggested that Sirt1-mediated deacetylation of FoxO1 and upregulation of Rab7 play an important role in mediating starvation-induced increases in autophagic flux, which in turn plays an essential role in maintaining left ventricular function during starvation.
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Silent Information Regulator 1 Protects the Heart From Ischemia/Reperfusion

TL;DR: In this article, the authors examined whether Sirt1 is protective against myocardial ischemia/reperfusion (I/R) in transgenic mice with cardiac-specific overexpression.
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Oxidative Stress Stimulates Autophagic Flux During Ischemia/Reperfusion

TL;DR: Results suggest that oxidative stress plays an important role in mediating autophagy during I/R, and that activation ofAutophagy through oxidative stress mediates myocardial injury in response to I/ R in the mouse heart.
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Nicotinamide phosphoribosyltransferase regulates cell survival through NAD+ synthesis in cardiac myocytes

TL;DR: Nampt critically regulates NAD+ and ATP contents, thereby playing an essential role in mediating cell survival by inhibiting apoptosis and stimulating autophagic flux in cardiac myocytes.