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The role and mechanism study of Cxcl14 in chronic critically ill cardiac dysfunction

Yongke Zheng1, Nanyuan Gu2, Kai Qiu2

  • 1Department of Rehabilitation, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, 261 Huansha Road, 310006, Hangzhou, Zhejiang, China.

Biochemical and Biophysical Research Communications
|February 26, 2025
PubMed

Insights

Chemokine Cxcl14 worsens cardiac dysfunction in chronic critical illness (CCI) by promoting inflammation and fibrosis. Neutralizing Cxcl14 offers a potential therapeutic strategy for CCI-related heart failure.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Critical Care Medicine

Background:

  • Chronic critical illness (CCI) is associated with significant cardiac dysfunction.
  • The specific mechanisms underlying CCI-induced heart problems require further elucidation.

Purpose of the Study:

  • To investigate the role and mechanism of Chemokine Cxcl14 (Cxcl14) in cardiac function impairment in patients with CCI.
  • To explore Cxcl14 as a potential therapeutic target for CCI-related cardiac dysfunction.

Main Methods:

  • Clinical data analysis of CCI patients with and without heart failure.
  • ELISA quantification of serum Cxcl14 levels.
  • Establishment of a CCI mouse model (CLP) to assess cardiac function, myocardial injury, inflammation, and fibrosis.
  • Evaluation of the therapeutic effect of anti-Cxcl14 antibody in the mouse model.

Main Results:

  • Serum Cxcl14 levels positively correlated with N-terminal pro-brain natriuretic peptide (NT-proBNP) and negatively with left ventricular ejection fraction (LVEF) in CCI patients.
  • In the CLP model, Cxcl14 reduced LVEF and left ventricular intramural shortening fraction (LVFS), increased markers of myocardial fibrosis (α-SMA, collagen III), and promoted inflammatory cell infiltration (ED-1, MPO, TNF-α, IL-6).
  • Administration of anti-Cxcl14 antibody ameliorated CCI-induced cardiac dysfunction.

Conclusions:

  • Cxcl14 expression is positively associated with the onset and severity of cardiac dysfunction in CCI.
  • Cxcl14 exacerbates myocardial injury and fibrosis while promoting inflammation in a CCI mouse model.
  • Targeting Cxcl14 with antibodies presents a promising therapeutic avenue for managing cardiac dysfunction in CCI.
Abstract

Keywords:
CCICardiac dysfunctionCxcl14FibrosisMyocardial injury

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