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Isolation of Functional Cardiac Immune Cells
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Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy.

Kathryn D Hok1, Haydn E Rich1, Anthony Shadid1

  • 1Center for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for Prevention of Human Diseases, UTHealth-McGovern Medical School, Houston, TX 77030, USA.

International Journal of Molecular Sciences
|October 29, 2025
PubMed
Summary
This summary is machine-generated.

Cardiac hypertrophy, a pathological response to heart damage, can be inhibited by targeting the complement system. This immune pathway plays a key role in inflammation and cardiac remodeling, offering new therapeutic targets.

Keywords:
autoimmune diseasescardiac arrhythmiascardiac hypertrophycardiac inflammationcardiac remodelingcardiovascular adversitiescardiovascular diseasescardiovascular eventscomplement anaphylatoxinscomplement immune systemcomplement in metabolic diseasesgenetic defects in complement genesinfectious diseases

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Medicine

Background:

  • Cardiac inflammation and hypertrophy are pathological responses to various insults, increasing cardiovascular mortality.
  • Inhibition of cardiac hypertrophy is crucial for reducing deaths from arrhythmias, heart failure, and sudden cardiac death.
  • The complement system, a key immune mediator, is implicated in cardiac damage and hypertrophy development.

Purpose of the Study:

  • To comprehensively review the role of the complement system's classical, lectin, and alternative pathways in cardiac inflammation and hypertrophy.
  • To discuss the involvement of complement pathways in various diseases contributing to cardiac damage.
  • To provide an overview of clinical trials targeting the complement system for cardiovascular mortality prevention.

Main Methods:

  • Literature review of scientific articles and clinical trial data.
  • Analysis of the roles of complement pathways in infectious, chronic inflammatory, genetic, and metabolic diseases.
  • Examination of current treatments and emerging anti-complement therapeutics.

Main Results:

  • All three complement activation pathways contribute to cardiac damage, inflammation, and hypertrophy.
  • Complement dysregulation is linked to various conditions causing cardiac pathology.
  • Clinical trials targeting the complement system show potential for preventing cardiovascular mortality.

Conclusions:

  • The complement system is a significant driver of cardiac inflammation and hypertrophy.
  • Emerging anti-complement therapeutics offer a promising strategy to inhibit the inflammatory response underlying cardiac hypertrophy.
  • Targeting the complement system may represent a future therapeutic approach beyond current RAAS-focused treatments.