MicroRNAs in Cancer Treatment-Induced Cardiotoxicity.
Laura PellegriniSara SilenoMarco D'AgostinoEleonora FoglioMaria Cristina FlorioVincenzo GuzzantiMatteo Antonio RussoFederica LimanaAlessandra MagentaPublished in: Cancers (2020)
Cancer treatment has made significant progress in the cure of different types of tumors. Nevertheless, its clinical use is limited by unwanted cardiotoxicity. Aside from the conventional chemotherapy approaches, even the most newly developed, i.e., molecularly targeted therapy and immunotherapy, exhibit a similar frequency and severity of toxicities that range from subclinical ventricular dysfunction to severe cardiomyopathy and, ultimately, congestive heart failure. Specific mechanisms leading to cardiotoxicity still remain to be elucidated. For instance, oxidative stress and DNA damage are considered key players in mediating cardiotoxicity in different treatments. microRNAs (miRNAs) act as key regulators in cell proliferation, cell death, apoptosis, and cell differentiation. Their dysregulation has been associated with adverse cardiac remodeling and toxicity. This review provides an overview of the cardiotoxicity induced by different oncologic treatments and potential miRNAs involved in this effect that could be used as possible therapeutic targets.
Keyphrases
- oxidative stress
- heart failure
- dna damage
- diabetic rats
- cell death
- cell proliferation
- left ventricular
- cell cycle arrest
- ischemia reperfusion injury
- prostate cancer
- transcription factor
- emergency department
- signaling pathway
- endoplasmic reticulum stress
- drug induced
- atrial fibrillation
- cardiac resynchronization therapy
- risk assessment
- minimally invasive
- chemotherapy induced