Metabolic Syndrome Mediates ROS-miR-193b-NFYA-Dependent Downregulation of Soluble Guanylate Cyclase and Contributes to Exercise-Induced Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction.

doi:10.1161/CIRCULATIONAHA.121.053889

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Metabolic Syndrome Mediates ROS-miR-193b-NFYA-Dependent Downregulation of Soluble Guanylate Cyclase and Contributes to Exercise-Induced Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction.

Circulation - 24 Aug 2021

Satoh Taijyu, Wang Longfei, Espinosa-Diez Cristina, Wang Bing, Hahn Scott A, Noda Kentaro, Rochon Elizabeth R, Dent Matthew R, Levine Andrea R, Baust Jeffrey J, Wyman Samuel, Wu Yijen L, Triantafyllou Georgios A, Tang Ying, Reynolds Mike, Shiva Sruti, Hilaire Cynthia St, Gomez Delphine, Goncharov Dmitry A, Goncharova Elena A, Chan Stephen Y, Straub Adam C, Lai Yen-Chun, McTiernan Charles F, Gladwin Mark T

Abstract excerpt

BACKGROUND: Many patients with heart failure with preserved ejection fraction have metabolic syndrome and develop exercise-induced pulmonary hypertension (EIPH). Increases in pulmonary vascular resistance in patients with heart failure with preserved ejection fraction portend a poor prognosis; this phenotype is referred to as combined precapillary and postcapillary pulmonary hypertension (CpcPH). Therapeutic...

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PMID: 34157861
DOI: 10.1161/CIRCULATIONAHA.121.053889
PMCID: PMC8384699

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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