Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
November 22, 2024Cell & BioscienceOpen Access

Splicing factor SRSF1 attenuates cardiomyocytes apoptosis via regulating alternative splicing of Bcl2L12

View Full Paper
Ask AI
Bookmark
Share

Key result

SRSF1 overexpression improved cardiac function and reduced infarct size in acute myocardial infarction mice by regulating Bcl2L12 alternative splicing to suppress cardiomyocyte apoptosis.

Why the study?

The function and mechanism of serine/arginine splicing factor 1 (SRSF1) in cardiovascular diseases remain unclear.

Does SRSF1 overexpression reduce cardiomyocyte apoptosis and infarct size in a mouse model of acute myocardial infarction?

Population

AMI mice and cardiomyocytes

Comparison

SRSF1 overexpression vs controls

Design

In vivo animal and in vitro cellular mechanistic study

Authors

YXYilin XieZYZhenbo YangWCWenxian Chen

Discussion

Loading...

Member takes

Overview

Hypothesis-generating for SRSF1 in murine AMI; leaves open translation to human ischemic disease.

Structured PICO

Does SRSF1 overexpression reduce cardiomyocyte apoptosis and infarct size in a mouse model of acute myocardial infarction?

P
Population
Preclinical study using male C57BL/6 mice and H9C2 cells to investigate the role of SRSF1 in cardiomyocyte apoptosis following acute myocardial infarction.
I
Intervention
Adeno-associated virus serotype 9 (AAV9) carrying the SRSF1 gene via tail vein injection (in vivo); SRSF1 overexpression plasmids or siRNAs (in vitro).
C
Comparator
Empty AAV9 vector and sham operation (in vivo); negative control siRNAs or empty vectors (in vitro).
O
Outcome
Cardiac function (left ventricular ejection fraction and fractional shortening), infarct size (TTC staining), and cardiomyocyte apoptosis (TUNEL staining, Bax, Bcl2, Cleaved-Caspase3 levels).surrogate

SRSF1 overexpression attenuates cardiomyocyte apoptosis and improves cardiac function post-myocardial infarction by regulating Bcl2L12 alternative splicing, highlighting a potential therapeutic target for ischemic heart disease.

Limitations

  • Bcl2L12 may not be the only downstream gene involved in SRSF1-mediated regulation of cardiomyocyte apoptosis.
  • Experimental models were limited to rats and mice, requiring further exploration to understand functions in the human heart.

Cite This Study

Xie et al. (2024) studied Acute myocardial infarction. SRSF1 overexpression (AAV9-SRSF1) vs. Empty AAV9 vector was evaluated on Cardiomyocyte apoptosis and cardiac function. SRSF1 overexpression improved cardiac function and reduced infarct size in acute myocardial infarction mice by regulating Bcl2L12 alternative splicing to suppress cardiomyocyte apoptosis.

synapsesocial.com/papers/6a7b7e79bdf697b3de02f9e2https://doi.org/10.1186/s13578-024-01324-3
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1SRSF1 inhibits autophagy through regulating Bcl-x splicing and interacting with PIK3C3 in lung cancer2021 · 131 citations
  2. 2Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastoma2008 · 145 citations
  3. 3Splicing factor BUD31 promotes ovarian cancer progression through sustaining the expression of anti-apoptotic BCL2L122022 · 41 citations
  4. 4LncRNA Chaer Prevents Cardiomyocyte Apoptosis From Acute Myocardial Infarction Through AMPK Activation2021 · 15 citations