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Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Engineered Regulatory T Lymphocytes Promote Infarcted Heart Repair.

Min Zhang1, Yongying Qin1, Ting Zhou1

  • 1Department of Cardiology, Hubei Key Laboratory of Biological Targeted Therapy, Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (M.Z., Y.Y.Q., T.Z., M.L.L., T.T.T., N.X., S.F.N., B.J.L., Z.F.Z., J.J., M.Y.G., J.Y.L., X.C.).

Circulation
|December 29, 2025
PubMed
Summary
This summary is machine-generated.

Engineered regulatory T cells (Tregs) targeting fibroblast activation protein (FAP) improve cardiac repair after myocardial infarction (MI). This novel therapy reduces fibrosis and inflammation by delivering interleukin-10 (IL-10) to injured heart tissue.

Keywords:
T-lymphocytes, regulatoryinterleukin-10myocardial infarctionreceptors, chimeric antigen

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Area of Science:

  • Cardiovascular Research
  • Immunotherapy
  • Regenerative Medicine

Background:

  • Myocardial infarction (MI) leads to poor cardiac healing with fibrosis and inflammation.
  • Regulatory T lymphocytes (Tregs) aid cardiac repair but struggle to reach damaged heart tissue.
  • Fibroblast activation protein (FAP)-specific chimeric antigen receptor (CAR) engineering aims to improve Treg delivery to infarct zones.

Purpose of the Study:

  • To investigate the therapeutic potential of FAP-specific CAR-engineered Tregs (FCTRs) for improving cardiac repair post-MI.
  • To determine the mechanisms by which FCTRs mediate therapeutic effects, focusing on IL-10 and Areg.
  • To assess the safety and efficacy of FCTRs in preclinical models of cardiac injury.

Main Methods:

  • Murine models of MI and ischemia-reperfusion injury were used.
  • Lentivirus-engineered FAP CAR Tregs (FCTRs) were administered intravenously.
  • Cardiac function, fibrosis, inflammation, and systemic toxicity were analyzed.
  • Studies utilized wild-type, IL-10 knockout, and Areg knockout Treg donors.

Main Results:

  • FCTRs successfully engrafted in injured cardiac tissue, improving cardiac function by day 14 post-MI.
  • Treatment with FCTRs significantly reduced cardiac fibrosis and inflammation without causing tissue damage.
  • Therapeutic efficacy was dependent on IL-10 production, which suppressed myofibroblast differentiation and promoted M2 macrophage polarization.
  • Areg ablation did not impair FCTR efficacy, and no adverse effects were observed.

Conclusions:

  • FAP-targeted CAR Tregs represent a dual-action precision therapy for post-MI recovery.
  • This approach resolves fibrosis and inflammation via IL-10-dependent mechanisms.
  • The strategy prevents maladaptive remodeling, accelerates functional recovery, and offers a platform for fibrotic diseases.