Effects of psychosocial stress on myocardial injury by modulating endoplasmic reticulum stress-induced autophagy and inflammation.

Psychosocial stress, a known trigger for depression, activates the sympathetic nervous system and serves as an independent risk factor for cardiovascular disease (CVD). However, its underlying mechanisms remain unclear. Endoplasmic reticulum stress (ERS), a protective response to stress, is linked to mental disorders. In depression patients, levels of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3), nuclear factor kappa-B (NF-κB), and interleukin-1β (IL-1) were elevated, while HRV parameters were reduced. Social defeat stress was found to activate autonomic neural activity, subsequently leading to myocardial injury through ERS modulation. Dopamine (DA), 5-hydroxytryptamine (5-HT), and corticosterone (CORT) levels were measured by ELISA. The number and morphology of amygdala neurons were evaluated via Nissl and TUNEL staining. ERS-induced autophagy and inflammation were assessed using western blot and immunofluorescence staining. This study links ERS to myocardial injury, suggesting ERS modulation could represent a potential therapeutic strategy for stress-induced myocardial injury.