HSP27 role in cardioprotection by modulating chemotherapeutic doxorubicin-induced cell death.
Sivasubramanian RamaniSung Kwon ParkPublished in: Journal of molecular medicine (Berlin, Germany) (2021)
The common phenomenon expected from any anti-cancer drug in use is to kill the cancer cells without any side effects to non-malignant cells. Doxorubicin is an anthracycline derivative anti-cancer drug active over different types of cancers with anti-cancer activity but attributed to unintended cytotoxicity and genotoxicity triggering mitogenic signals inducing apoptosis. Administration of doxorubicin tends to both acute and chronic toxicity resulting in cardiomyopathy (left ventricular dysfunction) and congestive heart failure (CHF). Cardiotoxicity is prevented through administration of different cardioprotectants along with the drug. This review elaborates on mechanism of drug-mediated cardiotoxicity and attenuation principle by different cardioprotectants, with a focus on Hsp27 as cardioprotectant by prevention of drug-induced oxidative stress, cell survival pathways with suppression of intrinsic cell death. In conclusion, Hsp27 may offer an exciting/alternating cardioprotectant, with a wider study being need of the hour, specifically on primary cell line and animal models in conforming its cardioprotectant behaviour.
Keyphrases
- cell death
- cell cycle arrest
- heart failure
- drug induced
- left ventricular
- heat shock protein
- oxidative stress
- drug delivery
- heat stress
- adverse drug
- heat shock
- blood pressure
- cancer therapy
- induced apoptosis
- nitric oxide
- endoplasmic reticulum stress
- emergency department
- acute coronary syndrome
- coronary artery disease
- cell proliferation
- hepatitis b virus
- intensive care unit
- electronic health record
- stress induced
- hypertrophic cardiomyopathy
- left atrial
- acute heart failure
- water soluble