ReviewPulmonary circulation2025
The Role of the Pulmonary Vascular Microenvironment in Chronic Thromboembolic Pulmonary Hypertension.
Review in Pulmonary circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Chronic Thromboembolic Pulmonary Hypertension as an Inflammation-Angiogenesis Disorder: From Thrombus Persistence to Dual Pulmonary Vasculopathy.Reviews in cardiovascular medicine · 2026Review
- Single-cell transcriptomics reveals NDRG1/TGF‑β1 associated vascular smooth muscle cell phenotypic switching in chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by persistent obstruction and vascular remodeling of the pulmonary arteries following pulmonary thromboembolism (PTE), diagnosed after a minimum of 3 months of therapeutic anticoagulation. Disease progression from PTE to CTEPH takes place in the pulmonary circulation, where the vascular microenvironment is composed of a fluid portion that includes blood cells and components of the fibrinolytic system, and various vascular cells, including endothelial and smooth muscle cells. Following PTE, the homeostasis of the pulmonary vascular microenvironment is disrupted, leading to the accumulation of inflammatory mediators and immune cells at the site of thrombosis. Platelets are also involved in the regulation of coagulation and inflammation, and functional changes such as impaired fibrinolysis are observed. Subsequently, endothelial cell dysfunction and smooth muscle cell dysregulation lead to delayed thrombus resolution and pulmonary vascular remodeling, eventually resulting in CTEPH. Early intervention targeting the aberrant vascular microenvironment may thwart or mitigate the transition from PTE to CTEPH. Here, we discuss the development of CTEPH from the perspective of the pulmonary vascular microenvironment and examine its related biomarkers and therapeutic methods for CTEPH diagnosis and treatment.
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