Evidence map›Paper›PMID 39576398›Full record

ArticleNeurochemical research2024

Chaperone-Mediated Autophagy Alleviates Cerebral Ischemia-Reperfusion Injury by Inhibiting P53-Mediated Mitochondria-Associated Apoptosis.

Shaonan Yang, Lu Jiang, Ling Deng, Jingjing Luo, Xiaoling Zhang, Sha Chen, Zhi Dong

Abstract read
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In one paragraph

Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Shaonan Yang *Key Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Lu Jiang *Key Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Ling DengKey Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Jingjing LuoKey Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Xiaoling ZhangKey Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China.
Sha ChenKey Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China. 191037@cqmu.edu.cn.
Zhi DongKey Laboratory of Biochemistry and Molecular Pharmacology, Department of Pharmacology, Chongqing Medical University, Chongqing, 400016, China. 100798@cqmu.edu.cn.

Funding

China Postdoctoral Science Foundation Project 220MD713710Chongqing Science Technology Commission CSTB2022NSCQ-MSX1097Chongqing Yuzhong District Science Technology Commission of China 20210121Key Project for Technological Innovation and Application Development in Chongqing CSTB2022TIAD-KPX0147the Chongqing Postdoctoral Special funding of Chongqing Human Resources and Social Security Bureau 2021XM3063the Science and Technology Research Program of Chongqing Municipal Education Commission KJQN202200458
6 · The paper itself

Abstract

Ischemia-reperfusion is a complex brain disease involving multiple biological processes, including autophagy, oxidative stress, and mitochondria-associated apoptosis. Chaperone-mediated autophagy (CMA), a selective autophagy, is involved in the development of various neurodegenerative diseases and acute nerve injury, but its role in ischemia-reperfusion is unclear. Here, we used middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R) models to simulate cerebral ischemic stroke in vivo and in vitro, respectively. LAMP2A (lysosome-associated membrane protein 2A), a key molecule of CMA, was dramatically downregulated in ischemia-reperfusion. Enhancement of CMA activity by LAMP2A overexpression reduced the neurological deficit, brain infarct volume, pathological features, and neuronal apoptosis of the cortex in vivo. Concomitantly, enhanced CMA activity alleviated OGD/R-induced apoptosis and mitochondrial membrane potential decline in vitro. In addition, we found that CMA inhibited the P53(Tumor protein p53) signaling pathway and reduced P53 translocation to mitochondria. The P53 activator, Nutlin-3, not only reversed the inhibitory effect of CMA on apoptosis, but also significantly weakened the protective effect of CMA on OGD/R and MCAO/R. Taken together, these results indicate that inhibition of P53-mediated mitochondria-associated apoptosis is essential for the neuroprotective effect of CMA against ischemia-reperfusion.

Indexed as

ApoptosisChaperone-Mediated AutophagyInfarction, Middle Cerebral ArteryMitochondriaRats, Sprague-DawleyReperfusion InjuryTumor Suppressor Protein p53AnimalsBrain IschemiaLysosomal-Associated Membrane Protein 2MaleRatsLysosomal-Associated Membrane Protein 2Tumor Suppressor Protein p53Chaperone-mediated autophagyIschemia–reperfusionNeuronal deathTumor protein p53

Identifiers

PMID39576398

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.