Targeting macrophage subsets for infarct repair

Tamar Ben-Mordechai1, Dahlia Palevski1, Yifat Glucksam-Galnoy2

  • 1Sackler Faculty of Medicine, Neufeld Cardiac Research Institute, Tel Aviv University, Tel Aviv, Israel Tamman Cardiovascular Research Institute, Leviev Heart Center, Sheba Medical Center, Tel-hashomer, Israel Sheba Center for Regenerative Medicine, Stem Cell, and Tissue Engineering, Tel-Hashomer, Israel.

Insights

Targeting macrophages, key players in cardiovascular disease, offers a promising therapeutic strategy. Modulating their function, particularly after myocardial infarction, can enhance natural heart repair and regeneration processes.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Regenerative Medicine

Background:

  • Macrophages are central to all cardiovascular diseases and present a significant therapeutic target.
  • Macrophage behavior (activation, plasticity, heterogeneity) is complex, influencing outcomes as beneficial or detrimental.
  • Macrophages play a critical role in healing and repair post-myocardial infarction, making them a focus for theranostic applications.

Purpose of the Study:

  • To review recent advances in targeting and modulating macrophage function for improved myocardial infarct repair.
  • To explore macrophage polarization, plasticity, heterogeneity, and their interactions with mesenchymal cells in infarct repair.
  • To highlight the potential of in situ macrophage targeting, particularly using liposomes, for regenerative therapies.

Main Methods:

  • Literature review focusing on recent discoveries in macrophage targeting and modulation.
  • Analysis of macrophage polarization, plasticity, and heterogeneity in the context of myocardial infarction.
  • Examination of macrophage cross-talk with mesenchymal cells during repair processes.
  • Focus on liposome-based in situ targeting strategies for macrophages.

Main Results:

  • Macrophages are crucial for regulating healing and repair after myocardial infarction.
  • Macrophage plasticity allows for switching between subsets, impacting repair outcomes.
  • Targeting macrophages in situ, potentially with liposomes, shows promise for enhancing repair.
  • Modulating macrophage function could reactivate endogenous myocardial regeneration programs.

Conclusions:

  • Targeting and modulating macrophage function represent a viable strategy to improve infarct repair and cardiac regeneration.
  • Understanding macrophage plasticity and heterogeneity is key to developing effective theranostic approaches.
  • In situ targeting methods, such as liposomes, offer a promising avenue for enhancing endogenous regenerative capabilities in the heart.

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