Evidence map›Paper›PMID 31712309›Full record

ArticleThe Journal of biological chemistry2019

BMP10 preserves cardiac function through its dual activation of SMAD-mediated and STAT3-mediated pathways.

Xiuxia Qu, Ying Liu, Dayan Cao, Jinghai Chen, Zhuo Liu, Hongrui Ji, Yuwen Chen, Wenjun Zhang, Ping Zhu, Deyong Xiao and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

39 citing papers in PubMed, 49 citations in OpenAlex.

  1. Diagnostic and prognostic utility of bone morphogenetic protein 10 in acute dyspnea: a cohort study.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
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  9. Bone morphogenetic protein 10: clinical correlates and risk of incident atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2025
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  11. SHP2 genetic variants in NSML-associated RASopathies disrupt the PZR-IRX transcription factor signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 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

13 authors at 6 institutions in 2 countries.

Xiuxia QuWuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China.
Ying LiuHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Dayan CaoInstitute of Materia Medica and Center of Translational Medicine, College of Pharmacy, Army Medical University, Chongqing 400038, China.ORCID 0000-0001-7648-3668
Jinghai ChenDepartment of Cardiology, the Second Affiliate Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang 310029, China.
Zhuo LiuHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Hongrui JiHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Yuwen ChenHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Wenjun ZhangHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Ping ZhuHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Deyong XiaoHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Xiaohui LiInstitute of Materia Medica and Center of Translational Medicine, College of Pharmacy, Army Medical University, Chongqing 400038, China lps008@aliyun.com.
Weinian ShouHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202 wshou@iu.edu.
Hanying ChenHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202 hanchen@iu.edu.
Indiana University School of MedicineArmy Medical University · CNGuangdong Academy of Medical Sciences · CNHarbin University of Science and Technology · CNJiangnan University · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

Transcriptional regulation of cardiac morphogenesisP01HL134599 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Lei Yang · 2017 to 2026
$25.7M
REGULATION OF CARDIOMYOCYTE SURVIVALP01HL085098 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2007 to 2011
$10.9M
Transcriptional regulation of cardiac conduction system morphogenesisR01HL145060 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI FIRULLI, ANTHONY B., SHOU, WEINIAN · 2019 to 2022
$2.8M
Molecular Pathway in Myocardium DevelopmentR01HL081092 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SHOU, WEINIAN · 2007 to 2011
$1.9M
The Role of BMP-10 in Cardiac DevelopmentR01HL070259 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SHOU, WEINIAN · 2002 to 2005
$1.3M
NHLBI NIH HHS P01 HL085098NHLBI NIH HHS P01 HL134599NHLBI NIH HHS R01 HL070259NHLBI NIH HHS R01 HL081092NHLBI NIH HHS R01 HL145060
6 · The paper itself

Abstract

Bone morphogenetic protein 10 (BMP10) is a cardiac peptide growth factor belonging to the transforming growth factor β superfamily that critically controls cardiovascular development, growth, and maturation. It has been shown that BMP10 elicits its intracellular signaling through a receptor complex of activin receptor-like kinase 1 with morphogenetic protein receptor type II or activin receptor type 2A. Previously, we generated and characterized a transgenic mouse line expressing BMP10 from the α-myosin heavy chain gene promoter and found that these mice have normal cardiac hypertrophic responses to both physiological and pathological stimuli. In this study, we report that these transgenic mice exhibit significantly reduced levels of cardiomyocyte apoptosis and cardiac fibrosis in response to a prolonged administration of the β-adrenoreceptor agonist isoproterenol. We further confirmed this cardioprotective function with a newly generated conditional Bmp10 transgenic mouse line, in which Bmp10 was activated in adult hearts by tamoxifen. Moreover, the intraperitoneal administration of recombinant human BMP10 was found to effectively protect hearts from injury, suggesting potential therapeutic utility of using BMP10 to prevent heart failure. Gene profiling and biochemical analyses indicated that BMP10 activates the SMAD-mediated canonical pathway and, unexpectedly, also the signal transducer and activator of transcription 3 (STAT3)-mediated signaling pathway both

Indexed as

Adrenergic beta-3 Receptor AgonistsAnimalsApoptosisBone Morphogenetic ProteinsExtracellular MatrixHeartHumansIsoproterenolMaleMiceMice, Inbred C3HMice, TransgenicMyocardiumMyocytes, CardiacRecombinant ProteinsSignal TransductionAdrenergic beta-3 Receptor AgonistsBMP10 protein, humanBone Morphogenetic ProteinsIsoproterenolRecombinant ProteinsSmad ProteinsSTAT3 Transcription Factorbone morphogenetic protein (BMP)cell deathfibrosisheart failureSMAD transcription factorSTAT transcription factor

Identifiers

PMID31712309
PMCPMC6937579
OpenAlexW2983692475

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.