RBM27 regulates cardiac function and diseases by maintaining the alternative splicing of Tnnt2 transcript

Q: What is the clinical evidence from this study?

Population: Myocardial infarction-induced heart failure and dilated cardiomyopathy. Intervention: Cardiomyocyte-specific overexpression or deletion of RBM27. Primary outcome: Cardiac function and alternative splicing of Tnnt2.

Q: What does this research mean for the field?

The RNA-binding protein RBM27 protects against heart failure and maintains cardiac function by directly regulating the alternative splicing of the Tnnt2 transcript. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Cong Qin; Zhiguo Zhang; Meiwei Zhang; Xinzhi Li; Zhengbin Han; Zhenzhi Li; Xueliang Wang; Zhiguo Zhang; Jingpeng Jin; Shanshan Zhou; Zheng Chen

doi:10.1016/j.gendis.2026.102434

September 1, 2026Genes & DiseasesOpen Access

RBM27 regulates cardiac function and diseases by maintaining the alternative splicing of Tnnt2 transcript

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Key result

RBM27 overexpression ameliorates post-MI heart failure, while deletion causes dilated cardiomyopathy via Tnnt2 exon skipping.

Why the study?

Correct mRNA splicing is critical for heart function, but the molecular mechanisms and role of RNA-binding proteins in this process remain largely unclear.

Key Points

To determine the function and molecular mechanism of the RNA-binding protein RBM27 in cardiac alternative mRNA splicing and heart failure.
Generated cardiomyocyte-specific Rbm27 knockout and overexpression mouse models subjected to myocardial infarction.
Assessed cardiac structure and function alongside alternative splicing of Tnnt2 transcript exon 11, with rescue experiments using full-length TNNT2 and mutant TNNT2Δexon11.
Cardiomyocyte-specific deletion of Rbm27 caused dilated cardiomyopathy and heart failure driven by Tnnt2 exon 11 skipping, which was rescued by wild-type TNNT2.
Cardiomyocyte-specific RBM27 overexpression attenuated myocardial infarction-induced heart failure, with direct binding of RBM27's RNA recognition motif to Tnnt2 exon 11 essential for splicing regulation.

Structured PICO

P

Population

Preclinical mouse models including myocardial infarction-induced heart failure models, cardiomyocyte-specific RBM27 overexpression mice, and cardiomyocyte-specific Rbm27 deletion (Rbm27-CKO) mice

I

Intervention

Cardiomyocyte-specific overexpression or deletion of RBM27, and TNNT2 rescue

C

Comparator

Control mice (implied)

O

Outcome

Cardiac function, development of heart failure or dilated cardiomyopathy, and alternative splicing of Tnnt2surrogate

RBM27 plays a critical role in maintaining cardiac function and preventing heart failure by regulating the alternative splicing of Tnnt2.

Implication

RBM27 splicing modulation may influence post-MI remodeling; leaves open whether it represents a viable human therapeutic target.

Abstract

Correct mRNA splicing is important for maintaining heart function, and dysregulation of this process can result in heart failure. However, the molecular mechanisms underlying this process, particularly the role of RNA-binding protein (RBP) in regulating mRNA splicing, remain largely unclear. We identified RBM27 as an important regulator of cardiac function and diseases. Abnormal RBM27 expression was associated with myocardial infarction-induced heart failure. Cardiomyocyte-specific overexpression of RBM27 ameliorated myocardial infarction-induced heart failure, whereas cardiomyocyte-specific deletion of Rbm27 led to dilated cardiomyopathy and heart failure due to exon11 skipping in Tnnt2 . TNNT2, but not TNNT2Δexon11, rescued heart failure in Rbm27 -CKO mice. The RNA recognition motif (RRM) of RBM27 was essential for maintaining cardiac function by ensuring normal alternative splicing of Tnnt2 . RBM27 bound directly to the exon 11 region of Tnnt2 mRNA. These findings demonstrate that RBM27 plays a critical role in heart function by maintaining the normal alternative splicing of Tnnt2 , highlighting its importance in maintaining heart health.

Discussion

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Cite This Study

Qin et al. (2026) studied Myocardial infarction-induced heart failure and dilated cardiomyopathy. Cardiomyocyte-specific overexpression or deletion of RBM27 was evaluated on Cardiac function and alternative splicing of Tnnt2. Cardiomyocyte-specific overexpression of RBM27 ameliorated myocardial infarction-induced heart failure, whereas its deletion led to dilated cardiomyopathy due to Tnnt2 exon11 skipping.

synapsesocial.com/papers/6a99353a636c6408cfa7d3ae https://doi.org/10.1016/j.gendis.2026.102434

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RBM27 regulates cardiac function and diseases by maintaining the alternative splicing of Tnnt2 transcript

Key Points

Structured PICO

Implication

Abstract

Discussion

Cite This Study

RBM27 regulates cardiac function and diseases by maintaining the alternative splicing of Tnnt2 transcript

Key Points

Structured PICO

Implication

Abstract

Discussion

Cite This Study

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