Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date

Traian Chiuariu1,2, Delia Șalaru1,2, Carina Ureche1,2

  • 1Department of Internal Medicine, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 University Street, 700115 Iasi, Romania.

Insights

Cardiovascular disease and chronic kidney disease often coexist, driven by organ fibrosis in cardio-renal syndrome. This review explores molecular mechanisms and therapeutic targets for cardiac and renal fibrosis.

Area of Science:

  • Nephrology
  • Cardiology
  • Fibrosis Research

Background:

  • Cardiovascular disease (CVD) and chronic kidney disease (CKD) frequently coexist, significantly impacting patient outcomes.
  • Organ fibrosis is a key factor in cardio-renal syndrome (CRS) pathogenesis, leading to high rates of heart failure and sudden cardiac death.
  • Mechanisms include hemodynamic changes, renin-angiotensin-aldosterone system (RAAS) activation, FGF23, Klotho protein, and collagen deposition.

Purpose of the Study:

  • To review the molecular mechanisms underlying cardiac and renal fibrosis in patients with CKD and heart failure (HF).
  • To highlight emerging therapeutic targets and alternative strategies for managing cardio-renal fibrosis.

Main Methods:

  • Literature review focusing on molecular mechanisms of fibrosis in CKD and HF.
  • Analysis of proposed mediators and pathways contributing to fibroblast and collagen turnover.
  • Identification of novel therapeutic targets and agents.

Main Results:

  • Fibrosis significantly contributes to the progression of cardio-renal syndrome.
  • Multiple molecular pathways, including RAAS, FGF23, and Klotho, are implicated in cardiac and renal fibrosis.
  • Several novel therapeutic strategies are under investigation.

Conclusions:

  • Understanding the molecular basis of fibrosis is crucial for managing patients with coexisting CVD and CKD.
  • Targeting specific fibrotic pathways offers promising therapeutic avenues for cardio-renal conditions.
  • Further research into novel agents like RAAS inhibitors, serelaxin, and IL-11 antibodies is warranted.

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