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Hengyi Xiao

Researcher at Sichuan University

Publications -  24
Citations -  8044

Hengyi Xiao is an academic researcher from Sichuan University. The author has contributed to research in topics: Autophagy & Senescence. The author has an hindex of 16, co-authored 24 publications receiving 6305 citations.

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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

The Crosstalk Between Nrf2 and AMPK Signal Pathways Is Important for the Anti-Inflammatory Effect of Berberine in LPS-Stimulated Macrophages and Endotoxin-Shocked Mice

TL;DR: The results demonstrate convergence between AMPK and Nrf2 pathways and this intersection is essential for anti-inflammatory effect of BBR in LPS-stimulated macrophages and endotoxin-shocked mice.
Journal ArticleDOI

Anti-tumour Strategies Aiming to Target Tumour-Associated Macrophages

TL;DR: Recent advances in TAM‐targeted strategies for tumour therapy are summarized and four strategies are grouped into four categories: inhibiting macrophage recruitment; suppressing TAM survival; enhancing M1‐like tumoricidal activity of TAMs; blocking M2‐ like tumour‐promoting activity of Tams.
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Autophagy impairment with lysosomal and mitochondrial dysfunction is an important characteristic of oxidative stress-induced senescence

TL;DR: It is found that mitochondrial dysfunction plays an initiating role, while lysosomal dysfunction is more directly responsible for autophagy impairment and senescence, and the effect of rapamycin on autophagic flux is linked to its role in functional revitalization of both mitochondrial and lysOSomal functions.