ReviewMedical science monitor : international medical journal of experimental and clinical research2026
Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.
Review in Medical science monitor : international medical journal of experimental and clinical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Integrated Cytokine and Immune Cell Profiling Reveals a Distinct Immune Signature Associated with High-Altitude Pulmonary Edema.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-altitude pulmonary hypertension (HAPH) is a debilitating condition caused by chronic hypobaric hypoxia at high altitudes, leading to progressive pulmonary vascular remodeling and right heart failure. The altitude-adapted immune microenvironment plays a pivotal but underappreciated role in HAPH progression: innate immune cells mediate early endothelial damage and proinflammatory signaling, while adaptive immune dysregulation sustains chronic inflammation. This review focuses on hypoxic-induced altitude-adapted immune microenvironment alterations - including immune cell phenotypic reprogramming, metabolic shifts, and spatial reorganization - and their roles in driving endothelial dysfunction, smooth muscle cell proliferation, and fibroblast activation. It also explores immune-cell crosstalk with vascular cells via paracrine signaling/extracellular vesicles, and highlights therapeutic strategies. This article aims to review the roles of hypoxia, inflammation, and oxidative stress in vascular remodeling in HAPH.
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Registered trials
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