Evidence map›Paper›PMID 40091832›Full record

ArticleThe Journal of clinical investigation2025

Macrophages: key conductors behind perivascular inflammation and vascular remodeling in hypoxia-induced pulmonary hypertension.

Edda Spiekerkoetter

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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  6. 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

1 author.

Edda Spiekerkoetter

Funding

Developmental Heterogeneity of Pulmonary Endothelial Phenotype at Single Cell ResolutionR01HL154002 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALVIRA, CRISTINA MARIA · 2021 to 2024
$2.8M
Understanding and targeting molecular and cellular events responsible for pulmonary arteriovenous malformation development, growth and regressionR01HL169787 · NHLBI · STANFORD UNIVERSITY · PI Edda Frauke Spiekerkoetter · 2023 to 2026
$2.8M
Lipid Peroxidation-Induced Mitochondrial Injury Inhibits Vascular Function in Single Ventricle Congenital Heart DiseaseR01HL165245 · NHLBI · STANFORD UNIVERSITY · PI Sushma Reddy · 2023 to 2026
$2.6M
Targeting Novel BMPR2 modifiers in Pulmonary Hypertension with Repurposed DrugsR01HL128734 · NHLBI · STANFORD UNIVERSITY · PI SPIEKERKOETTER, EDDA FRAUKE · 2016 to 2020
$2.1M
What triggers RV Fiber Re-Orientation in response to RV pressure overload, and what is its Consequence on Inter-Ventricular Decoupling?R01HL152250 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Vitaly Kheyfets · 2023 to 2026
$1.9M
Understanding and targeting molecular as well as structural events governing right ventricular adaptation, failure and recovery in pulmonary hypertension using repurposed drugsR01HL158868 · NHLBI · STANFORD UNIVERSITY · PI SPIEKERKOETTER, EDDA FRAUKE · 2021 to 2024
$1.7M
NHLBI NIH HHS R01 HL128734NHLBI NIH HHS R01 HL152250NHLBI NIH HHS R01 HL154002NHLBI NIH HHS R01 HL158868NHLBI NIH HHS R01 HL165245NHLBI NIH HHS R01 HL169787
6 · The paper itself

Abstract

Pulmonary hypertension (PH) encompasses a heterogenous group of disorders with the common feature of increased pulmonary arterial pressures. Patients with PH associated with lung disease and/or hypoxia undergo immune-mediated vascular remodeling that includes thickening of the muscular layer surrounding arteries and arterioles. In this issue of the JCI, Kumar and colleagues examined the role of interstitial macrophages in a model of high-altitude PH. Resident interstitial macrophages increased, proliferated, and expressed CCL2, a monocyte chemoattractant ligand. There was also a rise in CCR2+ macrophages expressing thrombospondin-1, which is known to activate vascular remodeling through TGF-β. Blocking monocyte recruitment partially reduced hypoxic PH, and corticosteroid treatment effectively reduced CCL2 expression and CCR2+ monocyte recruitment. Further, plasma samples collected from individuals ascending from low to high altitudes showed increased thrombospondin-1 and TGF-β levels, which were reduced with dexamethasone. These findings reveal interstitial macrophage populations as potential therapeutic targets in hypoxic PH.

Indexed as

Hypertension, PulmonaryHypoxiaMacrophagesVascular RemodelingAnimalsChemokine CCL2DexamethasoneHumansInflammationMiceThrombospondin 1Transforming Growth Factor betaCCL2 protein, humanChemokine CCL2DexamethasoneThrombospondin 1Transforming Growth Factor beta

Identifiers

PMID40091832
PMCPMC11910220

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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 OpenQuestion graph.