Potential Mechanisms of Sodium-Glucose Cotransporter 2 Inhibitors in Regulating Cardiac and Renal Fibrosis

Wei Huang1, Tianxiang Guan2,3, Ziyou Yan4

  • 1Department of Nephrology, Shenzhen Bao'an Authentic Traditional Chinese Medicine Therapy Hospital, Shenzhen, China.

Abstract

Insights

Sodium-glucose cotransporter 2 (SGLT2) inhibitors slow chronic kidney disease (CKD) progression by affecting renal tubules. This review explores how SGLT2 inhibitors may reduce cardiac and kidney fibrosis, offering cardiorenal protection.

Area of Science:

  • Nephrology
  • Cardiology
  • Pharmacology

Background:

  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors are novel therapeutics for diabetic kidney disease.
  • Emerging evidence suggests SGLT2 inhibitors slow chronic kidney disease (CKD) progression and reduce cardiovascular risk.
  • Cardiac and renal fibrosis are key pathological drivers of CKD and cardiovascular dysfunction.

Purpose of the Study:

  • To provide a comprehensive overview of the mechanisms by which SGLT2 inhibitors regulate cardiac and renal fibrosis.
  • To elucidate the molecular and cellular pathways involved in the antifibrotic effects of SGLT2 inhibitors.

Main Methods:

  • Literature review of preclinical and clinical studies on SGLT2 inhibitors and fibrosis.
  • Analysis of molecular and cellular mechanisms implicated in SGLT2 inhibitor-mediated antifibrotic effects.

Main Results:

  • SGLT2 inhibitors demonstrate potential in modulating cardiac and renal fibrosis.
  • Specific pathways targeted by SGLT2 inhibitors in fibrogenesis are under investigation.

Conclusions:

  • SGLT2 inhibitors may exert cardiorenal protective effects, partly through antifibrotic actions.
  • Further research is needed to fully elucidate the mechanisms underlying SGLT2 inhibitor-mediated antifibrosis.

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