Psychosocial stress in animal models is postulated to accelerate myocardial fibrosis via brain mitochondrial stress that activates extrinsic and intrinsic inflammatory pathways.
How does psychosocial stress intersect with the development of myocardial fibrosis in animal models?
Psychosocial stress may accelerate myocardial fibrosis and heart failure progression through brain mitochondrial stress and subsequent inflammatory pathway activation.
Psychosocial stress has been identified to increase the development and severity of cardiovascular disease, particularly heart failure. An underlying structural factor for the development and progression of certain forms of heart failure is the accumulation of extracellular matrix-generically termed myocardial fibrosis. However, it remains unclear what pathways and mechanisms by which psychosocial stress intersects with the development of myocardial fibrosis. This review will focus upon animal models of psychosocial stress and specific signaling pathways which may be relevant to the development of myocardial fibrosis. This includes sympathetic efferent activation, localized inflammatory pathways, mitochondrial stress, and a key cell type responsible for myocardial fibrosis, the fibroblast. Finally, the functional and clinical implications on how myocardial fibrosis contributes to heart failure and exacerbated by psychosocial stress will be examined. The main take away from this session was to identify different animal models of psychosocial stress/PTSD and find common mechanisms of signaling and inflammation. A unifying postulate was that mitochondrial stress within the brain can cause activation of extrinsic (cytokines) and intrinsic (inflammasome) inflammatory pathways which result in the emergence of a profibrotic fibroblast and acceleration of myocardial fibrosis.
Spinale et al. (Tue,) conducted a review in Psychosocial stress and myocardial fibrosis. Psychosocial stress was evaluated. Psychosocial stress in animal models is postulated to accelerate myocardial fibrosis via brain mitochondrial stress that activates extrinsic and intrinsic inflammatory pathways.