Evidence map›Paper›PMID 39142248›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2024

Emerging role of BMPs/BMPR2 signaling pathway in treatment for pulmonary fibrosis.

Qinmao Ye, Sarah J Taleb, Jing Zhao, Yutong Zhao

Abstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Identification of IPF specific genes expressed by lung tissue-derived fibroblasts using next generation sequencing.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Particulate matter increases bone morphogenetic protein 2 in lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
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

4 authors.

Qinmao YeDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, United States.
Sarah J TalebDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, United States.
Jing ZhaoDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, United States; Department of internal Medicine, the Ohio State University, Columbus, OH, United States.
Yutong ZhaoDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, United States; Department of internal Medicine, the Ohio State University, Columbus, OH, United States. Electronic address: yutong.zhao@osumc.edu.

Funding

Molecular regulation of immunoproteasome assembly in inflammatory diseasesR01HL167846 · NHLBI · OHIO STATE UNIVERSITY · PI JING ZHAO · 2023 to 2026
$2.4M
ISGylation regulates lung endothelial inflammationR01HL157164 · NHLBI · OHIO STATE UNIVERSITY · PI ZHAO, YUTONG · 2021 to 2024
$2.2M
Molecular regulation of BMPRII stability in lung fibrosisR01HL169203 · NHLBI · OHIO STATE UNIVERSITY · PI Yutong Zhao · 2023 to 2026
$2.0M
Molecular regulation of anti-inflammatory cytokine receptor in sepsisR01HL136294 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, YUTONG · 2018 to 2021
$1.8M
Deubiquitinating and inhibiting Hsp90 by USP40 mitigates lung injuryR01HL151513 · NHLBI · OHIO STATE UNIVERSITY · PI ZHAO, JING · 2020 to 2023
$1.7M
American Heart Association-American Stroke Association 24PRE1198621NHLBI NIH HHS R01 HL136294NHLBI NIH HHS R01 HL151513NHLBI NIH HHS R01 HL157164NHLBI NIH HHS R01 HL167846NHLBI NIH HHS R01 HL169203
6 · The paper itself

Abstract

Pulmonary fibrosis is a fatal and chronic lung disease that is characterized by accumulation of thickened scar in the lungs and impairment of gas exchange. The cases with unknown etiology are referred as idiopathic pulmonary fibrosis (IPF). There are currently no effective therapeutics to cure the disease; thus, the investigation of the pathogenesis of IPF is of great importance. Recent studies on bone morphogenic proteins (BMPs) and their receptors have indicated that reduction of BMP signaling in lungs may play a significant role in the development of lung fibrosis. BMPs are members of TGF-β superfamily, and they have been shown to play an anti-fibrotic role in combating TGF-β-mediated pathways. The impact of BMP receptors, in particular BMPR2, on pulmonary fibrosis is growing attraction to researchers. Previous studies on BMPR2 have often focused on pulmonary arterial hypertension (PAH). Given the strong clinical association between PAH and lung fibrosis, understanding BMPs/BMPR2-mediated signaling pathway is important for development of therapeutic strategies to treat IPF. In this review, we comprehensively review recent studies regarding the biological functions of BMPs and their receptors in lungs, especially focusing on their roles in the pathogenesis of pulmonary fibrosis and fibrosis resolution.

Indexed as

Bone Morphogenetic Protein Receptors, Type IIBone Morphogenetic ProteinsPulmonary FibrosisSignal TransductionAnimalsAntifibrotic AgentsHumansIdiopathic Pulmonary FibrosisLungAntifibrotic AgentsBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IIBone Morphogenetic ProteinsAnti-fibrosisBMP ligandsBMP receptorsMyofibroblast differentiationPro-fibrotic responsesPulmonary fibrosisTGF-β pathway

Identifiers

PMID39142248
PMCPMC11364484

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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.