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Article

Extracellular Cyclophilin A, Especially Acetylated, Causes Pulmonary Hypertension by Stimulating Endothelial Apoptosis, Redox Stress, and Inflammation.

Arteriosclerosis, thrombosis, and vascular biology - 1 Jun 2017

Xue Chao, Sowden Mark, Berk Bradford C

Abstract excerpt

OBJECTIVE: Oxidative stress and inflammation play key roles in the development of pulmonary arterial hypertension (PAH). Cyclophilin A (CypA) is secreted in response to oxidative stress and promotes inflammation and cardiovascular disease. Endothelial cell (EC) dysfunction is an early event in the pathogenesis of PAH. We evaluated the role of extracellular CypA in PAH and compared the effects of acetylated CypA...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 28450293
DOI: 10.1161/ATVBAHA.117.309212
PMCID: PMC5515294

Genes

PAH
ICAM1
VCAM1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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