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Chao-Yung Wang

Researcher at Chang Gung University

Publications -  85
Citations -  9650

Chao-Yung Wang is an academic researcher from Chang Gung University. The author has contributed to research in topics: Stent & Restenosis. The author has an hindex of 24, co-authored 83 publications receiving 7723 citations. Previous affiliations of Chao-Yung Wang include Brigham and Women's Hospital & Harvard University.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

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.
Journal ArticleDOI

Pleiotropic effects of statin therapy: molecular mechanisms and clinical results

TL;DR: Data from recent clinical trials are reviewed that support the concept of statin pleiotropy and provide a rationale for their clinical importance.
Book ChapterDOI

A mouse model of diet-induced obesity and insulin resistance.

TL;DR: The chapter describes protocols for diet induced-obesity model in mice and protocols for measuring insulin resistance and sensitivity, which are main contributors to the obesity trend in human.
Journal ArticleDOI

Decreased Perivascular Fibrosis but Not Cardiac Hypertrophy in ROCK1+/− Haploinsufficient Mice

TL;DR: Findings indicate ROCK1 is critical for the development of cardiac fibrosis, but not hypertrophy, in response to various pathological conditions and suggest that signaling pathways leading to the hypertrophic and profibrotic response of the heart are distinct.