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Xin Qi

Researcher at Case Western Reserve University

Publications -  68
Citations -  8989

Xin Qi is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Mitochondrial fission & Mitochondrion. The author has an hindex of 28, co-authored 61 publications receiving 7752 citations. Previous affiliations of Xin Qi include Stanford University & Hokkaido University.

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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

A novel Drp1 inhibitor diminishes aberrant mitochondrial fission and neurotoxicity.

Xin Qi, +3 more
- 01 Jan 2012 - 
TL;DR: The findings suggest that P110, as a selective peptide inhibitor of Drp1, might be useful for the treatment of diseases in which excessive mitochondrial fission and mitochondrial dysfunction occur.
Journal ArticleDOI

Inhibition of mitochondrial fragmentation diminishes Huntington’s disease–associated neurodegeneration

Xing Guo, +5 more
- 02 Dec 2013 - 
TL;DR: Data indicate that inhibition of DRP1-dependent excessive mitochondrial fission with a P110-TAT-like inhibitor may prevent or slow the progression of HD.
Journal ArticleDOI

Sodium 4-phenylbutyrate protects against cerebral ischemic injury.

Xin Qi, +4 more
- 01 Oct 2004 - 
TL;DR: The results indicate that 4-PBA could protect against cerebral ischemia through inhibition of ER stress-mediated apoptosis and inflammation, and its use as a chemical chaperone would provide a novel approach for the treatment of stroke.
Journal ArticleDOI

Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction

Marie Helene Disatnik, +6 more
- 08 Oct 2013 - 
TL;DR: It is shown that excessive mitochondrial fission at reperfusion contributes to long‐term cardiac dysfunction in rats and that acute inhibition of excessive mitochondrial h2O2 uncoupling state is sufficient to result in long-term benefits as evidenced by inhibiting cardiac dysfunction 3 weeks after acute myocardial infarction.