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Mechanisms with clinical implications for atrial fibrillation-associated remodeling: cathepsin K expression,

Masaya Fujita1, Xian W Cheng, Yasuya Inden

  • 1Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Journal of the American Heart Association
|December 18, 2013
PubMed

Insights

Elevated plasma cathepsin K (CatK) levels are linked to atrial fibrillation (AF). Angiotensin type 1 receptor antagonists may reduce fibrosis and CatK activation, potentially preventing AF.

Area of Science:

  • Cardiovascular Research
  • Biochemistry
  • Pathophysiology

Background:

  • Cathepsin K (CatK), a cysteine protease, is implicated in cardiovascular disease pathogenesis.
  • The relationship between atrial fibrillation (AF) and plasma CatK levels requires further investigation.
  • Understanding CatK's role in AF can identify new therapeutic targets.

Purpose of the Study:

  • To determine the association between atrial fibrillation (AF) and plasma CatK levels.
  • To investigate the expression and potential therapeutic targeting of CatK in AF.
  • To explore the role of angiotensin II signaling in CatK regulation in AF.

Main Methods:

  • Plasma CatK and ICTP levels were measured in 209 AF patients and 112 controls.
  • CatK expression was studied in vivo (tachypacing-induced AF in rabbits) and in vitro (rat neonatal myocytes).
  • Angiotensin type 1 receptor antagonist and MAPK inhibitors were used to assess therapeutic effects.

Main Results:

  • Patients with AF exhibited higher plasma CatK and ICTP levels compared to controls.
  • Persistent AF was associated with significantly higher CatK and ICTP levels than paroxysmal AF.
  • In rabbits, AF induced increased superoxide, CatK activity, fibrosis, and related molecular markers, which were reversed by angiotensin type 1 receptor antagonist.

Conclusions:

  • Increased plasma CatK levels are significantly associated with the presence of atrial fibrillation (AF).
  • Angiotensin type 1 receptor antagonism effectively reduced atrial fibrosis in a rabbit AF model.
  • Targeting CatK activation via angiotensin type 1 receptor blockade may represent a novel therapeutic strategy for preventing AF.
Abstract

Keywords:
angiotensin type 1 receptoratrial fibrillationcathepsin Kextracellular matrixmitogen‐activated protein kinase

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