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The crosstalk between STAT3 and microRNA in cardiac diseases and protection
Lan Wu1,2, Zhizheng Li3, Yanfei Li1,3
1Affiliated Zhoupu Hospital and Shanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Abstract:
Signal transducer and activator of transcription 3 (STAT3), an important transcription factor and signaling molecule, play an important role in cardiac disease and protection. As a transcription factor, STAT3 upregulates anti-oxidative and anti-apoptotic genes but suppresses anti-inflammatory and anti-fibrotic genes in cardiac disease and protection. As a signaling molecule, STAT3 is the downstream or upstream of other molecules for signaling transduction, also activated in cardiac disease and protection. MicroRNAs (miRNAs) are endogenous short non-coding RNAs that regulate mRNA expression at the transcriptional level and prevent protein translation. Recently, STAT3 is reported to be not only the target of miRNA but also the inhibitor or inducer of miRNA to modify the mRNA expression profiles in cardiomyocytes resulting in different effects on cardiac disease and protection. We summarize the current knowledge on STAT3 regulation of individual miRNAs and the modulation of STAT3 by miRNAs in cardiac diseases and protection.
Insights
Signal transducer and activator of transcription 3 (STAT3) influences cardiac disease and protection by regulating genes and signaling pathways. STAT3 also interacts with microRNAs (miRNAs), affecting gene expression in the heart.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Gene Regulation
Background:
- Signal transducer and activator of transcription 3 (STAT3) is a key transcription factor and signaling molecule involved in cardiac function.
- STAT3 modulates the expression of genes related to oxidative stress, apoptosis, inflammation, and fibrosis in the heart.
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression post-transcriptionally.
Purpose of the Study:
- To review the intricate relationship between STAT3 and miRNAs in the context of cardiac disease and protection.
- To elucidate how STAT3 regulates individual miRNAs and how miRNAs modulate STAT3 activity in cardiomyocytes.
- To understand the implications of these interactions on cardiac pathophysiology and therapeutic strategies.
Main Methods:
- Literature review and synthesis of existing research on STAT3 and miRNA interactions in cardiovascular contexts.
- Analysis of studies detailing STAT3's role as both a regulator and target of miRNAs.
- Examination of experimental evidence demonstrating altered mRNA expression profiles in cardiomyocytes due to STAT3-miRNA crosstalk.
Main Results:
- STAT3 acts as a transcription factor, upregulating protective genes (anti-oxidative, anti-apoptotic) and suppressing detrimental genes (anti-inflammatory, anti-fibrotic) in cardiac conditions.
- STAT3 is intricately linked with miRNAs, functioning as both a target and a modulator of miRNA expression.
- These interactions lead to significant modifications in mRNA expression within cardiomyocytes, impacting cardiac disease progression and protection.
Conclusions:
- The interplay between STAT3 and miRNAs represents a critical regulatory axis in cardiac disease and protection.
- Understanding this crosstalk is essential for deciphering complex cardiac signaling networks.
- Targeting the STAT3-miRNA axis may offer novel therapeutic avenues for cardiovascular diseases.
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