The impact of inflammation, neuromodulation and gut microbiota on developing cardiac fibrosis and hypertension - PubMed
5 hours ago
- #neuroimmune mechanisms
- #hypertension
- #cardiac fibrosis
- Cardiovascular diseases (CVD) are the leading cause of premature mortality worldwide, often starting with hypertension and progressing to heart failure.
- Cardiac fibrosis reduces functional cardiomyocytes and contraction force while increasing oxygen demand, driven by myofibroblasts producing excessive extracellular matrix.
- Immune cells, autonomic nervous system dysregulation, and sympathetic hyperactivity contribute to inflammation and fibrosis in hypertension and heart failure.
- Recent findings highlight molecular pathways involving immune activation, neuromodulation, epigenetic modifications, and gut microbiota in cardiac fibrosis.
- Potential therapeutic options include anti-inflammatory treatments, epigenetic modulators, and vagus nerve stimulation.
- Current heart failure treatments like RAA inhibitors, β-AR antagonists, SGLT2 inhibitors, and specific diets (DASH, Mediterranean) impact these processes at a molecular level.
- Understanding neuroimmune mechanisms is crucial, especially post-COVID-19, due to increased CVD risk from cytokine storms during SARS-CoV-2 infection.