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Small Extracellular Vesicles From Infarcted and Failing Heart Accelerate Tumor Growth.

Tal CallerItai RotemOlga Shaihov-TeperDaria LendengoltsYeshai ScharyRuty ShaiEfrat Glick-SaarDan DominissiniMenachem MotieiIdan KatzirRachela PopovtzerMerav NahmoudAlex BoomgardenCrislyn D'Souza-SchoreyNili Naftali-ShaniJonathan Leor
Published in: Circulation (2024)
Cardiac sEVs, specifically cMSC-sEVs from post-MI hearts, carry multiple protumorigenic factors. Uptake of cMSC-sEVs by cancer cells accelerates tumor growth. Treatment with spironolactone significantly reduces accelerated tumor growth after MI. Our results provide new insight into the mechanism connecting post-MI LVD to cancer and propose a translational option to mitigate this deadly association.
Keyphrases
  • papillary thyroid
  • heart failure
  • left ventricular
  • squamous cell
  • squamous cell carcinoma
  • combination therapy
  • lymph node metastasis