Psychological stress and myocardial extracellular matrix remodeling- a pathologic synergy

Area of Science:

• Cardiovascular Disease Research
• Neuroscience
• Pathology

Background:

• Psychosocial stress exacerbates cardiovascular disease, especially heart failure.
• Myocardial fibrosis, an extracellular matrix accumulation, underlies heart failure progression.
• The precise mechanisms linking psychosocial stress to myocardial fibrosis are not fully understood.

Purpose of the Study:

• To review animal models of psychosocial stress.
• To identify signaling pathways involved in stress-induced myocardial fibrosis.
• To examine the role of fibroblasts and inflammation in this process.

Main Methods:

• Analysis of animal models simulating psychosocial stress and PTSD.
• Investigation of sympathetic nervous system activation.
• Examination of inflammatory signaling (cytokines, inflammasomes) and mitochondrial stress.
• Focus on fibroblast activation and extracellular matrix deposition.

Main Results:

• Mitochondrial stress in the brain triggers both extrinsic and intrinsic inflammatory pathways.
• These pathways promote fibroblast activation, leading to a profibrotic state.
• Sympathetic efferent activation and localized inflammation are key mediators.

Conclusions:

• Psychosocial stress accelerates myocardial fibrosis through brain-initiated inflammatory signaling.
• This process involves mitochondrial dysfunction, fibroblast activation, and sympathetic nervous system involvement.
• Understanding these mechanisms is crucial for managing stress-related heart failure.