Liraglutide suppresses ferroptosis by upregulation NRF2 in type 2 diabetic cardiomyopathy.

Recent research indicates that inhibiting myocardial ferroptosis may help alleviate diabetic cardiomyopathy (DCM). Liraglutide (LIRA), a glucagon-like peptide-1 receptor agonist, has been shown to offer cardiovascular protective effects. Nevertheless, the specific role of LIRA and its relationship with myocardial ferroptosis in type 2 DCM is still not well understood.

Dapagliflozin attenuates diabetic cardiomyopathy via NRF2 protein upregulation-driven glutathione synthesis to inhibit myocardial ferroptosis.

Aims: Ferroptosis has emerged as a critical pathological mechanism contributing to the development and progression of type 2 diabetic cardiomyopathy (DCM). Dapagliflozin (DAPA), a sodium-glucose co-transporter 2 inhibitor (SGLT2i) with established cardiovascular benefits, however, DAPA's efficacy in modulating ferroptosis during type 2 DCM remains to be elucidated.

Methods And Fundings: In vivo, using a spontaneously diabetic Goto-Kakizaki (GK) rat model, we conducted proteomic profiling revealing distinct myocardial ferroptosis signatures associated with dysregulated glutathione metabolism across normal control, GK and GK + DAPA groups.

Identification of potential candidate genes and pathways in atrioventricular nodal reentry tachycardia by whole-exome sequencing.

Background: Atrioventricular nodal reentry tachycardia (AVNRT) is the most common manifestation of paroxysmal supraventricular tachycardia (PSVT). Increasing data have indicated familial clustering and participation of genetic factors in AVNRT, and no pathogenic genes related to AVNRT have been reported.

Methods: Whole-exome sequencing (WES) was performed in 82 patients with AVNRT and 100 controls.

Targeted next-generation sequencing identified a known mutation in a Chinese patient with Emery-Dreifuss muscular dystrophy.

Emery-Dreifuss muscular dystrophy (EDMD) is a rare X-linked recessive disease characterized by the clinical triad of early childhood joint contractures, progressive weakness in muscles and cardiac involvement and can result in sudden death. Targeted next-generation sequencing was performed for a Chinese patient with EDMD and the previously reported mutation [NM_000117.2: c.

Two pedigrees with arrhythmogenic right ventricular cardiomyopathy linked with R49H and F531C mutation in .

Arrhythmogenic right ventricular cardiomyopathy (ARVC) presents as the progressive fibrofatty replacement of the cardiomyocytes particularly in the right ventricular wall. Here, we report two cases with ARVC. In family A, the proband carries a () gene complex heterozygous mutation NM_001943.

Myocardial caspase-3 and NF-κB activation promotes calpain-induced septic apoptosis: The role of Akt/eNOS/NO pathway.

Aims: To explore the potential mechanism that the role of the Akt/eNOS/NO pathway in calpain-induced caspase-3 and NF-κB activation during septic apoptosis.

Main Methods: Septic rats were stimulated by LPS (8 mg/kg, i.p.