What does this research mean for the field?

Chronic severe aortic regurgitation drives progression to heart failure through coordinated transcriptional alterations in myocardial apoptosis, oxidative stress, metabolic regulation, and calcium-handling pathways. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To investigate myocardial transcriptional alterations and molecular pathways induced by chronic volume overload during the transition to decompensated eccentric hypertrophy in severe aortic regurgitation.

September 8, 2026International Journal of Molecular SciencesOpen Access

Left Ventricular Molecular Signature in Chronic Aortic Regurgitation

Q: What is the clinical evidence from this study?

Study design: Other. Population: Chronic aortic regurgitation (n=18). Intervention: Retrograde aortic valve perforation (induced chronic aortic regurgitation) vs. Age-matched control rats. Primary outcome: Cardiac remodeling and myocardial gene-expression profiling.

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Why the study?

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

Population

Male Wistar rats (n=18 total; 10 AR, 8 controls)

Comparison

Induction of severe aortic regurgitation by… vs Age-matched control rats

Design

Preclinical

Follow-up

60 days

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 Oumeiri LDLaurence Dewachter PBP. van de Borne

Discussion

Member takes

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?

Population

18 male Wistar rats (10 with induced severe aortic regurgitation and 8 age-matched controls) evaluated 60 days after surgery.

Intervention

Induction of severe aortic regurgitation (AR) by retrograde aortic valve perforation

Comparator

Age-matched control rats

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/6a9fc6ea684b366da041e528 https://doi.org/10.3390/ijms27177950

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September 8, 2026International Journal of Molecular SciencesOpen Access

Left Ventricular Molecular Signature in Chronic Aortic Regurgitation

View Full Paper

Ask AI

Bookmark

Why the study?

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

Population

Male Wistar rats (n=18 total; 10 AR, 8 controls)

Comparison

Induction of severe aortic regurgitation by… vs Age-matched control rats

Design

Preclinical

Follow-up

60 days

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 Oumeiri LDLaurence Dewachter PBP. van de Borne

Discussion

Member takes

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?

Population

18 male Wistar rats (10 with induced severe aortic regurgitation and 8 age-matched controls) evaluated 60 days after surgery.

Intervention

Induction of severe aortic regurgitation (AR) by retrograde aortic valve perforation

Comparator

Age-matched control rats

Outcome

Cardiac remodeling evaluated by echocardiography, invasive hemodynamics, and myocardial gene-expression profiling using RT-qPCRsurrogate

Cite This Study

synapsesocial.com/papers/6a9fc6ea684b366da041e528 https://doi.org/10.3390/ijms27177950

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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