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September 8, 2026International Journal of Molecular SciencesOpen Access

Left Ventricular Molecular Signature in Chronic Aortic Regurgitation

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Why the study?

Molecular mechanisms underlying the progression from compensated eccentric hypertrophy to heart failure in chronic aortic regurgitation remain poorly understood.

Does chronic severe aortic regurgitation induce specific transcriptional changes in the left ventricle in a rat model?

Population

Male Wistar rats (n = 10 with AR, n = 8 controls)

Comparison

Induced severe aortic regurgitation vs age-matched controls

Design

Experimental animal study

Key result

Chronic aortic regurgitation induced by retrograde aortic valve perforation in rats resulted in marked left ventricular dilatation, systolic dysfunction, and coordinated transcriptional changes.

Authors

BOBachar El OumeiriLDLaurence DewachterPBP. van de Borne

Discussion

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Overview

Rat AR model identifies transcriptional targets in decompensated remodeling; leaves open translation to human AR management.

Key Points

  • To investigate myocardial transcriptional alterations and molecular pathways induced by chronic volume overload during the transition to decompensated eccentric hypertrophy in severe aortic regurgitation.
  • Severe aortic regurgitation was surgically induced in male Wistar rats (n = 10) via retrograde aortic valve perforation and compared with age-matched controls (n = 8).
  • Cardiac remodeling was evaluated 60 days after surgery using echocardiography, invasive hemodynamics, and myocardial gene-expression profiling via RT-qPCR.
  • Chronic aortic regurgitation induced left ventricular dilatation and systolic dysfunction, confirming decompensated eccentric hypertrophy.
  • Gene expression analysis showed activation of pro-apoptotic signals with an increased BAX/BCL2 ratio, altered antioxidant defenses via decreased SOD2 and increased GPX1, and reduced SERCA2A expression reflecting impaired calcium handling.
  • Metabolic pathways were altered, evidenced by downregulated AMPKα1, PPARγ, and GLUT4, alongside upregulated OLR1, 15-LOX, and KLK10.

Structured PICO

Does chronic severe aortic regurgitation induce specific transcriptional changes in the left ventricle in a rat model?

P
Population
18 male Wistar rats (10 with induced severe aortic regurgitation and 8 age-matched controls) evaluated 60 days after surgery.
I
Intervention
Induction of severe aortic regurgitation (AR) by retrograde aortic valve perforation
C
Comparator
Age-matched control rats
O
Outcome
Cardiac remodeling evaluated by echocardiography, invasive hemodynamics, and myocardial gene-expression profiling using RT-qPCRsurrogate

Chronic aortic regurgitation in a rat model induces coordinated transcriptional alterations across multiple pathways implicated in myocardial dysfunction, providing potential molecular targets for future research.

Cite This Study

Oumeiri et al. (2026) studied Chronic aortic regurgitation (n=18). Retrograde aortic valve perforation (induced chronic aortic regurgitation) vs. Age-matched control rats was evaluated on Cardiac remodeling and myocardial gene-expression profiling. Chronic aortic regurgitation induced by retrograde aortic valve perforation in rats resulted in marked left ventricular dilatation, systolic dysfunction, and coordinated transcriptional changes.

synapsesocial.com/papers/6a9fc6ea684b366da041e528https://doi.org/10.3390/ijms27177950
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