What does this research mean for the field?

Srprb knockdown improves cardiac remodeling and reduces ventricular arrhythmias in heart failure mice, while overexpression worsens these outcomes. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the role and molecular mechanisms of signal recognition particle receptor beta subunit (Srprb) in cardiac structural and electrical remodeling and ventricular arrhythmia susceptibility during heart failure.

January 24, 2026Journal of the American Heart AssociationOpen Access

Signal Recognition Granule Receptor Beta Subunit Promotes Arrhythmogenic Remodeling in the Heart Failure Mice

Q: What are the key findings of this study?

Srprb knockdown improved cardiac remodeling and reduced ventricular arrhythmias in heart failure mice, while overexpression worsened these outcomes.

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Key result

Srprb knockdown improves cardiac remodeling and reduces ventricular arrhythmias in heart failure mice.

Why the study?

Heart failure is frequently complicated by ventricular arrhythmias that worsen prognosis, but the role of endoplasmic reticulum membrane-anchored Srprb in this process was unclear.

Does Srprb modulation affect arrhythmogenic remodeling and ventricular arrhythmia susceptibility in a mouse model of pressure overload-induced heart failure?

Population

Male C57BL/6 mice and primary neonatal mouse cardiomyocytes and fibroblasts

Comparison

Cardiac-specific Srprb overexpression vs knockdown

Design

Preclinical animal and in vitro mechanistic study

Follow-up

4 weeks post aortic banding

Authors

JZJ S ZhangWuhan University YPYucheng PanCardiovascular Institute Hospital YGYang GongUniversity of Macau

Discussion

Member takes

Implication

Hypothesis-generating for Srprb inhibition in experimental heart failure; leaves open human translation.

Key Points

To determine the role and molecular mechanisms of signal recognition particle receptor beta subunit (Srprb) in cardiac structural and electrical remodeling and ventricular arrhythmia susceptibility during heart failure.
Injected male C57BL/6 mice (n=6 per group) with adeno-associated virus vectors to achieve cardiac-specific Srprb knockdown or overexpression, followed 3 weeks later by aortic banding surgery.
Assessed cardiac structure, systolic function, surface electrocardiogram intervals, and ventricular arrhythmia inducibility using echocardiography, electrocardiography, and programmed electrical stimulation 4 weeks after aortic banding.
In vitro, transfected primary neonatal mouse ventricular cardiomyocytes and fibroblasts with adenoviral vectors to evaluate angiotensin II-induced hypertrophy and TGF-β-induced fibrosis.
Srprb expression was significantly elevated in human failing hearts, aortic-banded mouse hearts (P<0.01), and angiotensin II-treated primary cardiomyocytes (P<0.01).
In aortic-banded mice, Srprb knockdown significantly improved left ventricular ejection fraction (P<0.01) and fractional shortening (P<0.05), shortened QRS (P<0.05) and QTc (P<0.01) intervals, and reduced arrhythmia induction rate and duration (P<0.05).
Srprb overexpression exacerbated ventricular dilation, further decreased ejection fraction (P<0.05), and prolonged QRS (P<0.05) and QTc (P<0.05) intervals through endoplasmic reticulum stress and the TLR4/CaMKII/NF-κB pathway.

Structured PICO

Does Srprb modulation affect arrhythmogenic remodeling and ventricular arrhythmia susceptibility in a mouse model of pressure overload-induced heart failure?

Population

Male C57BL/6J wild-type mice aged approximately 6 weeks (weighing 18-20 g) subjected to pressure overload-induced heart failure via aortic banding, as well as primary neonatal mouse cardiomyocytes and fibroblasts.

Intervention

Tail vein injections of adeno-associated virus (AAV) to cardiac-specifically overexpress (AAV-Srprb) or knock down (AAV-Sh-Srprb) Srprb, administered 3 weeks prior to aortic banding. In vitro: adenovirus to overexpress or knock down Srprb.

Comparator

Sham surgery and negative control AAV/adenovirus vectors (AAV-NC, AAV-Sh-NC, Ad-NC, Ad-Sh-NC).

Outcome

Cardiac function, structural/electrical remodeling, and ventricular arrhythmia susceptibility evaluated 4 weeks post aortic banding.surrogate

Srprb promotes arrhythmogenic remodeling and ventricular arrhythmias in heart failure mice via endoplasmic reticulum stress and the TLR4/CaMKII/NF-κB pathway, identifying it as a potential therapeutic target.

Limitations

The precise mechanism by which Srprb regulates endoplasmic reticulum stress to promote ventricular arrhythmias remains elusive, necessitating further in-depth investigation.

Cite This Study

Zhang et al. (2026) studied this question. Srprb knockdown improved cardiac remodeling and reduced ventricular arrhythmias in heart failure mice, while overexpression worsened these outcomes.

synapsesocial.com/papers/6974616cbb9d90c67120b500 https://doi.org/10.1161/jaha.125.044103

Topics

Molecular Mechanisms of Cardiac Remodeling Heart failure HFrEF treatment

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January 24, 2026Journal of the American Heart AssociationOpen Access

Signal Recognition Granule Receptor Beta Subunit Promotes Arrhythmogenic Remodeling in the Heart Failure Mice

View Full Paper

Ask AI

Bookmark

Key result

Srprb knockdown improves cardiac remodeling and reduces ventricular arrhythmias in heart failure mice.

Why the study?

Heart failure is frequently complicated by ventricular arrhythmias that worsen prognosis, but the role of endoplasmic reticulum membrane-anchored Srprb in this process was unclear.

Does Srprb modulation affect arrhythmogenic remodeling and ventricular arrhythmia susceptibility in a mouse model of pressure overload-induced heart failure?

Population

Male C57BL/6 mice and primary neonatal mouse cardiomyocytes and fibroblasts

Comparison

Cardiac-specific Srprb overexpression vs knockdown

Design

Preclinical animal and in vitro mechanistic study

Follow-up

4 weeks post aortic banding

Authors

JZJ S ZhangWuhan University YPYucheng PanCardiovascular Institute Hospital YGYang GongUniversity of Macau

Discussion

Member takes

Implication

Hypothesis-generating for Srprb inhibition in experimental heart failure; leaves open human translation.

Key Points

To determine the role and molecular mechanisms of signal recognition particle receptor beta subunit (Srprb) in cardiac structural and electrical remodeling and ventricular arrhythmia susceptibility during heart failure.
Injected male C57BL/6 mice (n=6 per group) with adeno-associated virus vectors to achieve cardiac-specific Srprb knockdown or overexpression, followed 3 weeks later by aortic banding surgery.
Assessed cardiac structure, systolic function, surface electrocardiogram intervals, and ventricular arrhythmia inducibility using echocardiography, electrocardiography, and programmed electrical stimulation 4 weeks after aortic banding.
In vitro, transfected primary neonatal mouse ventricular cardiomyocytes and fibroblasts with adenoviral vectors to evaluate angiotensin II-induced hypertrophy and TGF-β-induced fibrosis.
Srprb expression was significantly elevated in human failing hearts, aortic-banded mouse hearts (P<0.01), and angiotensin II-treated primary cardiomyocytes (P<0.01).
In aortic-banded mice, Srprb knockdown significantly improved left ventricular ejection fraction (P<0.01) and fractional shortening (P<0.05), shortened QRS (P<0.05) and QTc (P<0.01) intervals, and reduced arrhythmia induction rate and duration (P<0.05).
Srprb overexpression exacerbated ventricular dilation, further decreased ejection fraction (P<0.05), and prolonged QRS (P<0.05) and QTc (P<0.05) intervals through endoplasmic reticulum stress and the TLR4/CaMKII/NF-κB pathway.

Structured PICO

Does Srprb modulation affect arrhythmogenic remodeling and ventricular arrhythmia susceptibility in a mouse model of pressure overload-induced heart failure?

Population

Intervention

Comparator

Sham surgery and negative control AAV/adenovirus vectors (AAV-NC, AAV-Sh-NC, Ad-NC, Ad-Sh-NC).

Outcome

Cardiac function, structural/electrical remodeling, and ventricular arrhythmia susceptibility evaluated 4 weeks post aortic banding.surrogate

Limitations

The precise mechanism by which Srprb regulates endoplasmic reticulum stress to promote ventricular arrhythmias remains elusive, necessitating further in-depth investigation.

Cite This Study

Zhang et al. (2026) studied this question. Srprb knockdown improved cardiac remodeling and reduced ventricular arrhythmias in heart failure mice, while overexpression worsened these outcomes.

synapsesocial.com/papers/6974616cbb9d90c67120b500 https://doi.org/10.1161/jaha.125.044103

Also Consider

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

Topics

Molecular Mechanisms of Cardiac Remodeling Heart failure HFrEF treatment

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