Evidence map›Paper›PMID 31659628›Full record

ArticleJournal of cell communication and signaling2020

CCN1 triggers adaptive autophagy in cardiomyocytes to curb its apoptotic activities.

Bor-Chyuan Su, Pei-Ling Hsu, Fan-E Mo

Open access · greenAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Bor-Chyuan SuDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 University Road, Tainan, 701, Taiwan.
Pei-Ling HsuDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 University Road, Tainan, 701, Taiwan.
Fan-E MoDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 University Road, Tainan, 701, Taiwan. femo@mail.ncku.edu.tw.ORCID http://orcid.org/0000-0002-0087-7043
National Cheng Kung University · TW

Funding

Ministry of Science and Technology of Taiwan 1062320B006043MY3
6 · The paper itself

Abstract

Autophagy occurs at basal levels for cellular homeostasis under normal conditions and is increased in response to nutrient starvation or stress to ensure cell survival. However, excessive autophagy can be deleterious to cardiomyocytes. CCN1/Cyr61, a matricellular protein, is expressed in the stressed heart to induce cardiomyopathy. The role of autophagy in CCN1-associated cardiotoxicity was not clear. Here, we found that autophagy was induced in the myocardium of the isoproterenol (ISO; 100 mg/kg/day for 5 days; s.c.) treated mice, where CCN1 expression is colocalized. The knock-in mice carrying an integrin α6β1-binding-defective mutant allele Ccn1-dm were resistant to the ISO-induced cardiac injury and autophagy. Our in vitro studies demonstrated that CCN1 dose- and time-dependently induced GFP-LC3-labeled autophagosome formation in rat cardiomyoblast H9c2 cells. The formation of autolysosomes in response to CCN1 (5 μg/ml; 3 h) treatment was identified by the acridine orange staining. The autophagy induction was confirmed by the elevated protein levels of Beclin 1, Atg5, and LC3-II, and the decrease of p62. Inhibition of autophagy by 3-methyladenine or by silencing Atg5 gene enabled CCN1-induced apoptosis in H9c2 cells, suggesting a protective role of autophagy. CCN1 binds to integrin α6β1 to induce autophagy through reactive oxygen species, and the activation of ERK and JNK. Furthermore, mitophagy was observed after CCN1 treatment for the clearance of depolarized mitochondria. Together, these results demonstrated that autophagy is induced in response to CCN1/α6β1 signaling in cardiomyocytes to alleviate CCN1-associated cardiotoxicity.

Indexed as

ApoptosisAutophagyCCN1Integrin α6β1Mitophagy

Identifiers

PMID31659628
PMCPMC7176774
OpenAlexW2982589979

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.