SGLT2 Inhibitor Might Prevent Atrial Fibrillation Related to Metabolic Syndrome via TNF-α Signaling Pathway: A...

Area of Science:

• Cardiovascular Research
• Pharmacology
• Bioinformatics

Background:

• Metabolic syndrome (MetS) increases atrial fibrillation (AF) risk.
• Sodium-glucose co-transporter 2 (SGLT2) inhibitors show potential in reducing AF risk.
• Mechanisms of SGLT2 inhibitors in MetS-related AF are not fully understood.

Purpose of the Study:

• To elucidate the mechanisms of SGLT2 inhibitors in preventing AF in MetS.
• To identify molecular targets and pathways affected by SGLT2 inhibitors in MetS-related AF.

Main Methods:

• Network pharmacology and bioinformatic analysis were used.
• Public databases (SwissTarget, GeneCards, OMIM, STRING) were utilized.
• Protein-protein interaction (PPI) networks, gene ontology (GO), and KEGG pathway analyses were performed.

Main Results:

• 52 common targets were identified between SGLT2 inhibitors and MetS-related AF.
• TNF-α and AGE-RAGE signaling pathways were highlighted as key mechanisms.
• p38 and JNK within the TNF-α pathway were identified as primary targets for reducing atrial remodeling and fibrosis.

Conclusions:

• SGLT2 inhibitors may mitigate AF in MetS through the TNF-α signaling pathway.
• Targeting TNF-α signaling presents a potential therapeutic strategy for MetS-related AF.
• Further experimental validation is required to confirm these findings.