Evidence map›Paper›PMID 35141256›Full record

ReviewFrontiers in medicine2021

Therapeutic Approaches for Treating Pulmonary Arterial Hypertension by Correcting Imbalanced TGF-β Superfamily Signaling.

Patrick Andre, Sachindra R Joshi, Steven D Briscoe, Mark J Alexander, Gang Li, Ravindra Kumar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  6. Review
  7. Article
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  9. Article
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  11. Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Growth factors involved in vascular remodeling in pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025
    Review
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Patrick AndreDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Sachindra R JoshiDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Steven D BriscoeDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Mark J AlexanderDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Gang LiDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Ravindra KumarDiscovery Group, Acceleron Pharma (a wholly-owned subsidiary of Merck & Co., Inc.), Cambridge, MA, United States.
Acceleron Pharma (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a rare disease characterized by high blood pressure in the pulmonary circulation driven by pathological remodeling of distal pulmonary arteries, leading typically to death by right ventricular failure. Available treatments improve physical activity and slow disease progression, but they act primarily as vasodilators and have limited effects on the biological cause of the disease-the uncontrolled proliferation of vascular endothelial and smooth muscle cells. Imbalanced signaling by the transforming growth factor-β (TGF-β) superfamily contributes extensively to dysregulated vascular cell proliferation in PAH, with overactive pro-proliferative SMAD2/3 signaling occurring alongside deficient anti-proliferative SMAD1/5/8 signaling. We review the TGF-β superfamily mechanisms underlying PAH pathogenesis, superfamily interactions with inflammation and mechanobiological forces, and therapeutic strategies under development that aim to restore SMAD signaling balance in the diseased pulmonary arterial vessels. These strategies could potentially reverse pulmonary arterial remodeling in PAH by targeting causative mechanisms and therefore hold significant promise for the PAH patient population.

Indexed as

activin ABMPBMPRIIcell proliferationPAHSMAD1/5/8SMAD2/3TGF-β

Identifiers

PMID35141256
PMCPMC8818880
OpenAlexW4207051255

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.