Evidence mapPaperPMID 40362501Full record

ReviewInternational journal of molecular sciences2025

Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.

Jinjin Dai, Hongyang Chen, Jindong Fang, Shiguo Wu, Zhuangzhuang Jia

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Murine Aortopulmonary Shunt Model of Flow-Driven Pulmonary Hypertension-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
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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

5 authors.

Jinjin DaiSchool of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.ORCID 0009-0000-7519-3706
Hongyang ChenSchool of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.ORCID 0000-0001-5452-8116
Jindong FangSchool of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.ORCID 0009-0007-7221-9887
Shiguo WuSchool of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.ORCID 0009-0006-1985-2010
Zhuangzhuang JiaSchool of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.ORCID 0000-0002-9376-6595

Funding

Zhuangzhuang Jia 202401AZ070001-022Zhuangzhuang Jia 82460923
6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a serious cardiovascular disease caused by a variety of pathogenic factors, which is characterized by increased pulmonary vascular resistance (PVR) and progressive elevation of mean pulmonary artery pressure (mPAP). This disease can lead to right ventricular hypertrophy and, in severe cases, right heart failure and even death. Vascular remodeling-a pathological modification involving aberrant vasoconstriction, cell proliferation, apoptosis resistance, and inflammation in the pulmonary vascular system-is a significant pathological hallmark of PH and a critical process in its progression. Recent studies have found that vascular remodeling involves the participation of a diversity of cellular pathological alterations, such as the dysfunction of pulmonary artery endothelial cells (PAECs), the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), the phenotypic differentiation of pulmonary artery fibroblasts, the inflammatory response of immune cells, and pericyte proliferation. This review focuses on the mechanisms and the intercellular crosstalk of these cells in the PH process, emphasizing recent advances in knowledge regarding cellular signaling pathways, inflammatory responses, apoptosis, and proliferation. To develop better treatments, a list of possible therapeutic approaches meant to slow down certain biological functions is provided, with the aim of providing new insights into the treatment of PH by simplifying the intricacies of these complex connections. In this review, comprehensive academic databases such as PubMed, Embase, Web of Science, and Google Scholar were systematically searched to discuss studies relevant to human and animal PH, with a focus on vascular remodeling in PH.

Indexed as

Hypertension, PulmonaryVascular RemodelingAnimalsApoptosisCell ProliferationEndothelial CellsHumansMyocytes, Smooth MusclePulmonary ArterySignal Transductioncellular mechanismsendothelial cellsfibroblastspulmonary hypertensionsmooth muscle cellsvascular remodeling

Identifiers

PMID40362501
PMCPMC12072204

What Socratic holds

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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.