Evidence mapPaperPMID 34135313Full record

ArticleCell death & disease2021

Osteocrin, a novel myokine, prevents diabetic cardiomyopathy via restoring proteasomal activity.

Xin Zhang, Can Hu, Xiao-Pin Yuan, Yu-Pei Yuan, Peng Song, Chun-Yan Kong, Teng Teng, Min Hu, Si-Chi Xu, Zhen-Guo Ma and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
10.0field-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

34 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  4. Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

11 authors at 1 institution in 1 country.

Xin Zhang *Department of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Can Hu *Department of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Xiao-Pin Yuan *Department of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Yu-Pei YuanDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Peng SongDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Chun-Yan KongDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Teng TengDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Min HuDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Si-Chi XuDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.
Zhen-Guo MaDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China. zhengma@whu.edu.cn.ORCID 0000-0002-0931-7536
Qi-Zhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China. qztang@whu.edu.cn.ORCID 0000-0003-2210-3169
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteasomal activity is compromised in diabetic hearts that contributes to proteotoxic stresses and cardiac dysfunction. Osteocrin (OSTN) acts as a novel exercise-responsive myokine and is implicated in various cardiac diseases. Herein, we aim to investigate the role and underlying molecular basis of OSTN in diabetic cardiomyopathy (DCM). Mice received a single intravenous injection of the cardiotrophic adeno-associated virus serotype 9 to overexpress OSTN in the heart and then were exposed to intraperitoneal injections of streptozotocin (STZ, 50 mg/kg) for consecutive 5 days to generate diabetic models. Neonatal rat cardiomyocytes were isolated and stimulated with high glucose to verify the role of OSTN in vitro. OSTN expression was reduced by protein kinase B/forkhead box O1 dephosphorylation in diabetic hearts, while its overexpression significantly attenuated cardiac injury and dysfunction in mice with STZ treatment. Besides, OSTN incubation prevented, whereas OSTN silence aggravated cardiomyocyte apoptosis and injury upon hyperglycemic stimulation in vitro. Mechanistically, OSTN treatment restored protein kinase G (PKG)-dependent proteasomal function, and PKG or proteasome inhibition abrogated the protective effects of OSTN in vivo and in vitro. Furthermore, OSTN replenishment was sufficient to prevent the progression of pre-established DCM and had synergistic cardioprotection with sildenafil. OSTN protects against DCM via restoring PKG-dependent proteasomal activity and it is a promising therapeutic target to treat DCM.

Indexed as

AnimalsApoptosisCells, CulturedCyclic GMP-Dependent Protein KinasesDiabetic CardiomyopathiesDisease Models, AnimalForkhead Box Protein O1MaleMiceMice, Inbred C57BLMuscle ProteinsMyocytes, CardiacPhosphorylationProof of Concept StudyProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktCyclic GMP-Dependent Protein KinasesForkhead Box Protein O1Foxo1 protein, mouseMuscle ProteinsOSTN protein, humanOstn protein, mouseOstn protein, ratProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktRecombinant ProteinsTranscription Factors

Identifiers

PMID34135313
PMCPMC8209005
OpenAlexW3171328573

What Socratic holds

Textmetadata
LicenceCC BY
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.