Regulatory T cells protect against diabetic cardiomyopathy in db/db mice.
Kai ZhangYunyi LiXiao GeLinlin MengJing KongXiao MengPublished in: Journal of diabetes investigation (2024)
Tregs ameliorated myocardial hypertrophy and fibrosis, improved cardiac dysfunction, and protected against DCM progression in db/db mice. The mechanisms involved a decrease of inflammatory response, oxidative stress and apoptosis, which might be mediated by phosphatidylinositol 3-kinase-protein kinase B and mitogen-activated protein kinase pathways. Hence, Tregs might serve as a promising therapeutic approach for DCM treatment.
Keyphrases
- protein kinase
- regulatory t cells
- oxidative stress
- inflammatory response
- high fat diet induced
- left ventricular
- dendritic cells
- type diabetes
- endoplasmic reticulum stress
- dna damage
- cell death
- ischemia reperfusion injury
- induced apoptosis
- diabetic rats
- wild type
- cell cycle arrest
- skeletal muscle
- adipose tissue
- toll like receptor
- signaling pathway
- replacement therapy
- atrial fibrillation
- liver fibrosis