Myocardial fibrosis & calcium overload
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Once the reactive oxygen species have been generated and AngII elevated much of the pathology is familiar, including micro vascular damage and regeneration, as per a recent detailed MRI study.
And we aren't even considering secondary autoimmune induced damage.
Pathogenesis and Prevention of Radiation-induced Myocardial Fibrosis (2017)
Oxidative stress
Free radicals and reactive oxygen species (ROS) are the important products of ionizing radiation on biological systems, where oxidative stress plays an important role in the mechanism of radiation effects. Substantial evidence indicates that chronic or acute overproduction of ROS is of great significance in the pathogenesis of cardiovascular disease. ROS can inactivate NO and the other vascular protective agents to prevent platelet aggregation, resulting in vascular endothelial dysfunction, and then induce or aggravate the occurrence of radiation-induced myocardial fibrosis. At the same time, oxidative stress directly induces the production of inflammatory factors, which can further increase the degree of radiation-induced myocardial fibrosis. NF-ÎșB is a protein complex that controls DNA transcription and participates in the cellâs response to stress, and it is a key link in oxidative stress and inflammatory pathways (Taunk et al., 2015).
Calcium overload
Angiotensin II increases intracellular calcium by activating the calcium channel on the fibroblast membrane. The expression of collagen type I and type III is enhanced, which further promotes the progression of myocardial fibrosis (Wang et al., 2012). Although its specific mechanism is not very clear, from the current level of research, it is possible that the intracellular calcium acts as a secondary messenger, affecting the formation of fibroblasts and promoting their proliferation. Furthermore, calcium ions play a role in promoting myocardial fibrosis by participating in some signal transduction pathways, which can promote the development of myocardial fibrosis.