Evidence map›Paper›PMID 32249716›Full record

ArticleAutophagy2021

The AMPK-MFN2 axis regulates MAM dynamics and autophagy induced by energy stresses.

Yongquan Hu, Hao Chen, Luying Zhang, Xiaoying Lin, Xia Li, Haixia Zhuang, Hualin Fan, Tian Meng, Zhengjie He, Haofeng Huang and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 1 pooled it
20.8field-weighted citation impact, top 1% of its field
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

190 citing papers in PubMed, 1 synthesis or guideline pooled it, 309 citations in OpenAlex.

  1. Pooled it
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University
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  20. NIBV Induces Incomplete Autophagy via AMPK-TFEB, Causing Kidney Injury in Chicks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article

130 more citing papers are in PubMed but not listed here.

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

16 authors at 6 institutions in 1 country.

Yongquan HuGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.ORCID 0000-0003-2699-1757
Hao ChenGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Luying ZhangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Xiaoying LinGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Xia LiGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Haixia ZhuangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Hualin FanGuangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, School of Medicine, South China University of Technology, Guangzhou, China.
Tian MengGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Zhengjie HeGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Haofeng HuangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.
Qing GongDepartment of Biochemistry and Molecular Biology, GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, People's Republic of China.
Dongxing ZhuGuangzhou Institute of Cardiovascular Diseases, the Second Affiliated Hospital, Key Laboratory of Cardiovascular Diseases, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China.ORCID 0000-0001-5419-438X
Yiming XuSchool of Basic Medical Sciences, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Guangzhou Medical University, Guangzhou, China.
Pengcheng HeDepartment of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Longxuan LiDepartment of Neurology, Gongli Hospital, Pudong New Area, Shanghai 219 Miaopu Road, Pudong New Area, Shanghai 200135, P. R. China.
Du FengGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, School of Basic Medical Sciences, Guangzhou Medical University, 511436, Guangzhou, China.ORCID 0000-0002-2489-4702
State Key Laboratory of Respiratory Disease · CNGuangdong Medical College · CNGuangdong Academy of Medical Sciences · CNGuangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Energy deprivation activates the cellular energy sensor AMP-activated protein kinase (AMPK), which in turn induces macroautophagy/autophagy. The mitochondrial-associated ER membrane (MAM) plays a key role in mitochondrial division and autophagy, and the mitochondrial fusion protein MFN2 (mitofusin 2) tethers the MAM, but the mechanism by which AMPK and MFN2 regulate autophagy in response to energy stress remains unclear. Here, we found that energy stress not only triggers mitochondrial fission and autophagy, but more importantly increases the number of MAMs, a process that requires AMPK. Interestingly, under energy stress, considerable amounts of AMPK translocate from cytosol to the MAM and the mitochondrion as mitochondrial fission occurs. Unexpectedly, AMPK interacts directly with MFN2. The autophagic ability of mouse embryonic fibroblasts (MEFs) lacking MFN2 (

Indexed as

AMP-Activated Protein KinasesAutophagosomesAutophagyEndoplasmic ReticulumFibroblastsHeLa CellsHumansMicrotubule-Associated ProteinsMitochondriaMitochondrial MembranesMitochondrial ProteinsMitophagyAMP-Activated Protein KinasesMicrotubule-Associated ProteinsMitochondrial ProteinsAMPKautophagyMAMmetforminMFN2mitochondrial fission

Identifiers

PMID32249716
PMCPMC8143230
OpenAlexW3014455336

What OpenQuestion 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 OpenQuestion graph.