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Related Experiment Video

Updated: Jun 30, 2025

Gene Transfer for Ischemic Heart Failure in a Preclinical Model
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Small Extracellular Vesicles From Infarcted and Failing Heart Accelerate Tumor Growth.

Tal Caller1,2, Itai Rotem1,2, Olga Shaihov-Teper1,2

  • 1Neufeld and Tamman Cardiovascular Research Institutes, School of Medicine, Tel Aviv University, Israel (T.C., I.R., O.S.-T., D.L., Y.S., R.S., M.N., N.N.-S., J.L.).

Circulation
|March 15, 2024
PubMed
Summary
This summary is machine-generated.

Cardiac small extracellular vesicles (sEVs) from hearts after myocardial infarction (MI) promote cancer growth. Treatment with spironolactone reduces this effect, offering a potential therapeutic strategy for the link between heart dysfunction and cancer.

Keywords:
cardio-oncologyextracellular vesiclesfibroblastsheart failureinflammationmesenchymal stem cellsmyocardial infarctionneoplasmsspironolactone

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Area of Science:

  • Cardiology
  • Oncology
  • Extracellular Vesicles Biology

Background:

  • Myocardial infarction (MI) and heart failure are linked to increased cancer incidence.
  • The underlying mechanisms connecting cardiac dysfunction and cancer remain unclear.
  • Cardiac small extracellular vesicles (sEVs) are investigated as a potential mediator.

Purpose of the Study:

  • To test the hypothesis that cardiac mesenchymal stromal cell-derived sEVs (cMSC-sEVs) link post-MI left ventricular dysfunction (LVD) to cancer.
  • To analyze the cargo and effects of cMSC-sEVs on cancer cells and tumor growth.
  • To evaluate spironolactone as a therapeutic intervention.

Main Methods:

  • Purification and characterization of sEVs from post-MI hearts and cultured cMSCs.
  • Proteomic analysis of cMSC-EV cargo.
  • In vitro assessment of cMSC-sEV effects on cancer cells, macrophages, and endothelial cells.
  • In vivo tumor modeling in mice with post-MI LVD, including sEV transfer and depletion studies.
  • Evaluation of spironolactone treatment.

Main Results:

  • Post-MI hearts and cMSCs produced more sEVs with tumor-promoting cargo compared to non-failing hearts.
  • cMSC-sEVs from post-MI hearts accelerated lung and colon cancer growth in vitro and in vivo.
  • Adoptive transfer of post-MI cMSC-sEVs increased tumor size and proliferation in mice with LVD.
  • sEV depletion reduced MI-associated tumor promotion, while spironolactone treatment suppressed tumor growth.

Conclusions:

  • Cardiac sEVs, particularly cMSC-sEVs, from post-MI hearts contain protumorigenic factors.
  • Uptake of these sEVs by cancer cells enhances tumor growth.
  • Spironolactone treatment effectively reduces accelerated tumor growth post-MI, suggesting a therapeutic avenue.