Mitochondrial SIRT2-mediated CPT2 deacetylation prevents diabetic cardiomyopathy by impeding cardiac fatty acid oxidation.

Dysregulated energy metabolism, particularly lipid metabolism disorders, has been identified as a key factor in the development of diabetic cardiomyopathy (DCM). Sirtuin 2 (SIRT2) is a deacetylase involved in the regulation of metabolism and cellular energy homeostasis, yet its role in the progression of DCM remains unclear. We observed significantly reduced SIRT2 expression in DCM model mice.

Nanoengineered therapeutic strategies targeting SNHG1 for mitigating microglial ischemia-reperfusion injury implications for hypoxic-ischemic encephalopathy.

The purpose of this work is to investigate the function of SNHG1, a long non-coding RNA implicated in disease progression, apoptosis, and proliferation, in order to solve the problem of hypoxic-ischemic encephalopathy (HIE) in newborn care. We investigated the impact of overexpressing SNHG1 on hypoxia-induced apoptosis and studied its expression in BV2 microglial cells under hypoxic circumstances. As a result of modifying YY1 expression, SNHG1's overexpression prevents apoptosis, as our data demonstrate that it is considerably downregulated under hypoxia.

Advances in cardiovascular-related biomarkers to predict diabetic peripheral neuropathy.

Diabetic peripheral neuropathy (DPN) is a common chronic complication of diabetes mellitus. One of the most common types is distal symmetric poly-neuropathy, which begins as bilateral symmetry pain and hyperesthesia and gradually progresses into hypoesthesia with nerve fibre disorder and is frequently accompanied by depression and anxiety. Notably, more than half of patients with DPN can be asymptomatic, which tends to delay early detection.