ArticleCirculation2026
Critical Contribution of Cardiac Myofibroblasts in Right Ventricular Failure and the Role of UCP2 SNPs in the Predisposition to RV Decompensation in Pulmonary Arterial Hypertension.
Article in Circulation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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13 authors.
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Abstract
backgroundRight ventricular failure drives both morbidity and mortality in pulmonary arterial hypertension (PAH), but the mechanism of transition from compensated right ventricle (cRV) to decompensated RV (dRV) is unknown, and some PAH patients develop dRV faster than others.
methodsWe explored the role of RV cardiac myofibroblasts (cMFBs) on this transition utilizing 2 rat models: monocrotaline (MCT) versus the less inflammatory pulmonary artery banding (PAB); and 3 patient cohorts (n=81) of PAH versus group 2 pulmonary hypertension (PHT-2). We hypothesized that loss of UCP2 (uncoupling protein 2), critical for mitochondrial calcium (mCa
resultsWe separated rat cRV from dRV based on catheterization and echocardiographic criteria and found a significant increase in cMFBs from MCT but not PAB RV (which decompensated much later than MCT RV). In isolated hearts, MCT RV contractility was lower in dRV but not in isolated cardiomyocytes (CMs), pointing to a non-CM cause. Mitochondrial respiration was lower in MCT dRV cMFBs than in control and cRV cFBs but increased in MCT-RV CMs. mCa
conclusionsOur data suggest that a change of cell identity (cFBs to cMFBs) in the RV is a driver of RV decompensation. TNF-α or rs659366 is a potential biomarker for early RV decompensation in PAH.
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