Evidence map›Paper›PMID 37345556›Full record

ArticleCirculation research2023

TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post-Myocardial Infarction by Inhibiting HDAC3.

Lin Weng, Jingjing Ye, Fenghe Yang, Shi Jia, Minghong Leng, Bo Jia, Chunling Xu, Yang Zhao, Ruxia Liu, Yufei Xiong and 3 more

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In one paragraph

Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
18.7field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Lin Weng *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Jingjing Ye *Trauma Medicine Center, Peking University People's Hospital, Key Laboratory of Trauma Treatment and Neural Regeneration (Peking University), National Center for Trauma Medicine, Beijing, China (J.Y., B.J.).ORCID 0009-0000-8906-4454
Fenghe YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Shi JiaDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Minghong LengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Bo JiaTrauma Medicine Center, Peking University People's Hospital, Key Laboratory of Trauma Treatment and Neural Regeneration (Peking University), National Center for Trauma Medicine, Beijing, China (J.Y., B.J.).
Chunling XuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).ORCID 0000-0002-7767-7605
Yang ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Ruxia LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Yufei XiongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Yiqing ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Junhui ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).
Ming ZhengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).ORCID 0000-0002-5797-1065
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgressive cardiac fibrosis leads to ventricular wall stiffness, cardiac dysfunction, and eventually heart failure, but the underlying mechanism remains unexplored. PDCD5 (programmed cell death 5) ubiquitously expresses in tissues, including the heart; however, the role of PDCD5 in cardiac fibrosis is largely unknown. Therefore, this study aims at exploring the possible role and underlying mechanisms of PDCD5 in the pathogenesis of cardiac fibrosis. METHODS AND

resultsPDCD5 levels were found to be elevated in the serum obtained from patients with cardiac fibrosis, in fibrotic mice heart tissues after myocardial infarction, and in cardiac fibroblasts stimulated by Ang II (angiotensin II)- or TGF-β1 (transforming growth factor-β1). Overexpression of PDCD5 in cardiac fibroblasts or treatment with PDCD5 protein reduced the expression of profibrogenic proteins in response to TGF-β1 stimulation, while knockdown of PDCD5 increased fibrotic responses. It has been demonstrated that SMAD3, a protein that is also known as mothers against decapentaplegic homolog 3, directly upregulated PDCD5 during cardiac fibrosis. Subsequently, the increased PDCD5 promoted HDAC3 (histone deacetylase 3) ubiquitination, thus, inhibiting HDAC3 to reduce fibrotic responses. Fibroblast-specific knock-in of PDCD5 in mice ameliorated cardiac fibrosis after myocardial infarction and enhanced cardiac function, and these protective effects were eliminated by AAV9-mediated HDAC3 overexpression.

conclusionsThe findings of this study demonstrated that PDCD5 is upregulated by SMAD3 during cardiac fibrosis, which subsequently ameliorated progressive fibrosis and cardiac dysfunction through HDAC3 inhibition. Thus, this study suggests that PDCD5 functions as a negative feedback factor on fibrotic signaling pathways and might serve as a potential therapeutic target to suppress the progression of fibrotic responses.

Indexed as

Myocardial InfarctionTransforming Growth Factor beta1AnimalsApoptosisFibroblastsFibrosisHeartMiceMyocardiumSmad3 ProteinSmad3 ProteinTransforming Growth Factor beta1cardiac dysfunctioncardiac fibrosisfibroblastsmyocardial infarctionnegative feedback factor

Identifiers

PMID37345556
OpenAlexW4381597294

What OpenQuestion holds

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Registered trials

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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.