Evidence map›Paper›PMID 33495814›Full record

ArticleMolecular medicine reports2021

H(+)/Cl(‑) exchange transporter 7 promotes lysosomal acidification‑mediated autophagy in mouse cardiomyocytes.

Jiezhi Lin, Jinyu Wei, Yanling Lv, Xingyue Zhang, Ruo Fan Yi, Chen Dai, Qiong Zhang, Jiezhi Jia, Dongxia Zhang, Yuesheng Huang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

10 authors at 2 institutions in 1 country.

Jiezhi Lin *Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Jinyu Wei *Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Yanling LvInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Xingyue ZhangInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Ruo Fan YiInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Chen DaiOrthopedics and Trauma Department, The 963rd (224th) Hospital of People's Liberation Army, 963rd Hospital of Joint Logistics Support Force of PLA, Jiamusi, Heilongjiang 154007, P.R. China.
Qiong ZhangInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Jiezhi JiaInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Dongxia ZhangInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Yuesheng HuangInstitute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Southwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy protects cardiomyocytes in various pathological and physiological conditions; however, the molecular mechanisms underlying its influence and the promotion of autophagic clearance are not completely understood. The present study aimed to explore the role of H(+)/Cl(‑) exchange transporter 7 (CLC‑7) in cardiomyocyte autophagy. In this study, rapamycin was used to induce autophagy in mouse cardiomyocytes, and the changes in CLC‑7 were investigated. The expression levels of CLC‑7 and autophagy‑related proteins, such as microtubule associated protein 1 light chain 3, autophagy related 5 and Beclin 1, were detected using western blotting or immunofluorescence. Autolysosomes were observed and analyzed using transmission electron microscopy and immunofluorescence following CLC‑7 silencing with small interfering RNAs. Cellular viability was assessed using Cell Counting Kit‑8 and lactate dehydrogenase assays. Lysosomal acidification was measured using an acidification indicator. Increased CLC‑7 co‑localization with lysosomes was identified during autophagy. CLC‑7 knockdown weakened the acidification of lysosomes, which are the terminal compartments of autophagy flux, and consequently impaired autophagy flux, ultimately resulting in cell injury. Collectively, the present study demonstrated that in cardiomyocytes, CLC‑7 may contribute to autophagy via regulation of lysosomal acidification. These findings provide novel insights into the role of CLC‑7 in autophagy and cytoprotection.

Indexed as

AutophagyAnimalsChloride ChannelsHydrogen-Ion ConcentrationLysosomesMiceMyocytes, CardiacChloride ChannelsClcn7 protein, mouseautophagycardiomyocyteCLC‑7lysosomal acidificationrapamycin

Identifiers

PMID33495814
PMCPMC7845584
OpenAlexW3124644753

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.