Evidence mapPaperPMID 39921526Full record

ReviewJournal of the American Heart Association2025

Skeletal Muscle Pathology in Pulmonary Arterial Hypertension and Its Contribution to Exercise Intolerance.

Thaís C F Menezes, Michael H Lee, Dara C Fonseca Balladares, Kevin Nolan, Sankalp Sharma, Rahul Kumar, Eloara V M Ferreira, Brian B Graham, Rudolf K F Oliveira

Abstract readReview
In one paragraph

Review in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Proteomic and metabolomic profiling nominates druggable targets and biomarkers for pulmonary arterial hypertension-associated myopathy and exercise intolerance in male monocrotaline rats.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025
    Article
  4. Article
  5. Article
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

9 authors.

Thaís C F MenezesDivision of Respiratory Diseases, Department of Medicine, Hospital São Paulo Federal University of São Paulo (UNIFESP) São Paulo Brazil.ORCID 0000-0003-4993-857X
Michael H LeeDivision of Pulmonary and Critical Care Medicine, Department of Medicine University of California, San Francisco San Francisco CA USA.ORCID 0000-0002-5739-8369
Dara C Fonseca BalladaresDivision of Pulmonary and Critical Care Medicine, Department of Medicine University of California, San Francisco San Francisco CA USA.ORCID 0009-0001-8427-5110
Kevin NolanDivision of Pulmonary and Critical Care Medicine, Department of Medicine University of California, San Francisco San Francisco CA USA.
Sankalp SharmaDepartment of Orthopaedic Surgery University of California San Francisco CA USA.
Rahul KumarDivision of Pulmonary and Critical Care Medicine, Department of Medicine University of California, San Francisco San Francisco CA USA.ORCID 0000-0002-2709-5981
Eloara V M FerreiraDivision of Respiratory Diseases, Department of Medicine, Hospital São Paulo Federal University of São Paulo (UNIFESP) São Paulo Brazil.ORCID 0000-0002-3291-6473
Brian B GrahamDivision of Pulmonary and Critical Care Medicine, Department of Medicine University of California, San Francisco San Francisco CA USA.ORCID 0000-0001-7541-2585
Rudolf K F OliveiraDivision of Respiratory Diseases, Department of Medicine, Hospital São Paulo Federal University of São Paulo (UNIFESP) São Paulo Brazil.ORCID 0000-0002-2252-8119

Funding

Activation, Phenotype and Function of CD4 T Cells in Schistosoma-Pulmonary HypertensionR01HL135872 · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2025 to 2025
$607k
The contribution of hypoxia inducible factor-1-dependent glycolysis in lung interstitial macrophages to the pathobiology of schistosomiasis-induced pulmonary hypertension.K08HL168310 · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2025 to 2025
$169k
NHLBI NIH HHS K08 HL168310NHLBI NIH HHS P01 HL152961NHLBI NIH HHS R01 HL135872
6 · The paper itself

Abstract

Pulmonary arterial hypertension is a disease of the pulmonary vasculature, resulting in elevated pressure in the pulmonary arteries and disrupting the physiological coordination between the right heart and the pulmonary circulation. Exercise intolerance is one of the primary symptons of pulmonary arterial hypertension, significantly impacting the quality of life. The pathophysiology of exercise intolerance in pulmonary arterial hypertension is complex and likely multifactorial. Although the significance of right ventricle impairment and perfusion/ventilation mismatch is widely acknowledged, recent studies suggest pathophysiology of the skeletal muscle contributes to reduced exercise capacity in pulmonary arterial hypertension, a concept explored herein.

Indexed as

Exercise ToleranceHypertension, PulmonaryMuscle, SkeletalPulmonary Arterial HypertensionAnimalsHumansPulmonary Arteryexercise intolerancemitochondrial dysfunctionoxygen pathwaypulmonary hypertensionskeletal muscle dysfunction

Identifiers

PMID39921526
PMCPMC12074786

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.