Abnormal mitochondrial functions are a major pathophysiological basis of diabetic cardiomyopathy. 5′ AMP-activated protein kinase (AMPK) is involved in mitochondrial dynamics. As an activator of AMPK, this study examined the effect of metformin on cardiomyocytes treated with high glucose. Primary cardiomyocytes isolated from neonatal rat ventricles were exposed to a high glucose concentration (33 mM) to establish a model of high-glucose injury with or without metformin (2 mM) treatment. AMPK activity was inhibited or activated by CC (20 µM) or AICAR (50 µM). CCK-8 and TUNEL assays were used to assess cell viability and apoptosis, respectively. A JC-1 assay was used to measure the mitochondrial membrane potential, and MitoSOX™ staining was used to examine mitoROS. Mito-Tracker Green-stained mitochondria were visualized by confocal microscopy to assess mitochondrial fission. Furthermore, we measured the expression levels of AMPK-mediated mitochondrial dynein and apoptotic proteins by western blotting. Our results showed that AMPK activity was significantly decreased in cardiomyocytes under the high-glucose condition, which was accompanied by increased mitochondrial fragmentation and aggravated mitochondrial dysfunction. The mitochondrial membrane potential was decreased and oxidative stress was increased, leading to apoptosis. Activation of AMPK by either metformin or AICAR reversed myocardial mitochondrial dysfunction and inhibited apoptosis under high glucose. Furthermore, inhibition of AMPK activity abrogated the protective effect of metformin against high glucose–induced mitochondrial dysfunction and apoptosis in cardiomyocytes. Our study demonstrates that metformin protects cardiomyocytes from high glucose–induced mitochondrial fragmentation and apoptosis by activating AMPK.

Pulmonary arterial hypertension (PAH) is a pathophysiological condition characterized by pulmonary vascular remodeling and elevated vascular resistance, which may ultimately result in cardiovascular failure and sudden cardiac death. In recent years, the occurrence of pregnancy complicated by pulmonary arterial hypertension has witnessed a notable increase, whereas the incidence of postpartum pulmonary arterial hypertension is comparatively rare. This study presents a case involving a 39-year-old female who exhibited severe pulmonary arterial hypertension, finally diagnosed as idiopathic pulmonary arterial hypertension, within 2 days postpartum. The diagnosis was made following a thorough clinical examination. This case report emphasizes the significance of promptly initiating targeted therapy as an initial step in effectively managing patients and the criticality of conducting a thorough assessment of multidisciplinary collaboration in postpartum management. Furthermore, the report has the potential to enhance awareness and education regarding the future management of similarly intricate conditions.