miR-93 and synaptotagmin-7: two novel players in the regulation of autophagy during cardiac hypertrophy.
Maurizio ForteGianmarco SartoSebastiano SciarrettaPublished in: The FEBS journal (2023)
The molecular mechanisms involved in the transition of cardiac hypertrophy to heart failure (HF) are not fully characterized. Autophagy is a catabolic, self-renewal intracellular mechanism, which protects the heart during HF. In the heart of a mouse model of angiotensin-II-induced hypertrophy, Sun and colleagues demonstrated that reduced levels of miR-93 lead to synaptotagmin-7 (Syt-7) upregulation and consequent inhibition of autophagy. miR-93 overexpression or syt-7 inhibition rescues autophagy and maladaptive hypertrophy. This research identifies new players in the pathophysiology of cardiac hypertrophy, opening innovative therapeutic perspectives. miR-93 may also be considered in the future as a novel circulating biomarker for patients at high risk to develop HF.
Keyphrases
- cell proliferation
- long non coding rna
- heart failure
- angiotensin ii
- cell death
- endoplasmic reticulum stress
- signaling pathway
- long noncoding rna
- mouse model
- oxidative stress
- acute heart failure
- end stage renal disease
- poor prognosis
- atrial fibrillation
- ejection fraction
- peritoneal dialysis
- vascular smooth muscle cells
- newly diagnosed
- left ventricular
- high glucose
- prognostic factors
- reactive oxygen species
- dna methylation
- drug induced
- cardiac resynchronization therapy
- endothelial cells
- patient reported
- stress induced