Cardiac inflammation and fibrosis following chemo/radiation therapy: mechanisms and therapeutic agents.
Run YangChangming TanMasoud NajafiPublished in: Inflammopharmacology (2021)
The incidence of cardiovascular disorders is one of the most concerns among people who underwent cancer therapy. The heart side effects of cancer therapy may occur during treatment to some years after the end of treatment. Some epidemiological studies confirm that heart diseases are one of the most common reasons for mortality among patients that were received treatment for cancer. Experimental studies and also clinical investigations indicate that inflammatory changes such as pericarditis, myocarditis, and also fibrosis are key mechanisms of cardiac diseases following chemotherapy/radiotherapy. It seems that chronic oxidative stress, massive cell death, and chronic overproduction of pro-inflammatory and pro-fibrosis cytokines are the key mechanisms of cardiovascular diseases following cancer therapy. Furthermore, infiltration of inflammatory cells and upregulation of some enzymes such as NADPH Oxidases are a hallmark of heart diseases after cancer therapy. In the current review, we aim to explain how radiation or chemotherapy can induce inflammatory and fibrosis-related diseases in the heart. We will explain the cellular and molecular mechanisms of cardiac inflammation and fibrosis following chemo/radiation therapy, and then review some adjuvants to reduce the risk of inflammation and fibrosis in the heart.
Keyphrases
- cancer therapy
- oxidative stress
- drug delivery
- radiation therapy
- induced apoptosis
- locally advanced
- heart failure
- cell death
- atrial fibrillation
- dna damage
- cardiovascular disease
- diabetic rats
- radiation induced
- risk factors
- liver fibrosis
- cell proliferation
- poor prognosis
- squamous cell carcinoma
- signaling pathway
- photodynamic therapy
- type diabetes
- metabolic syndrome
- case control
- heat shock
- cardiovascular risk factors
- childhood cancer