Int J Med Sci
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Diabetic cardiomyopathy (DC) is a pathophysiologic condition caused by diabetes mellitus (DM) in the absence of coronary artery disease, valvular heart disease, and hypertension that can lead to heart failure (HF), manifesting itself in the early stages with left ventricular hypertrophy and diastolic dysfunction, with marked HF and decreased systolic function in the later stages. There is still a lack of direct evidence to prove the exact existence of DC. ⋯ Several cell and animal studies have shown that ferroptosis is closely related to DC progression. This review systematically summarizes the related pathogenic mechanisms of ferroptosis in DC, including the reduction of cardiac RDH10 induced ferroptosis in DC cardiomyocytes which mediated by retinol metabolism disorders; CD36 overexpression caused lipid deposition and decreased GPX4 expression in DC cardiomyocytes, leading to the development of ferroptosis; Nrf2 mediated iron overload and lipid peroxidation in DC cardiomyocytes and promoted ferroptosis; lncRNA-ZFAS1 as a ceRNA, combined with miR-150-5p to inhibit CCND2 expression in DC cardiomyocytes, thereby triggering ferroptosis.
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Insulin resistance is the primary contributor to the disruption in glucose homeostasis in the body, playing a significant causative role in many metabolic diseases. Insulin resistance is characterized by compensatory insulin secretion and reduced insulin responsiveness in target organs. Dysregulation of the interaction between insulin-secreting cells and insulin-responsive target organs is an important factor driving the progression of insulin resistance. ⋯ In this review, we summarize the three types of hormones (classical hormones, organokines and extracellular vesicles) that play a regulatory role in insulin resistance, and focus on the novel endocrine hormones, extracellular vesicles, to elaborate the mechanism of extracellular vesicles' regulation of insulin resistance progress from two aspects: the impact on insulin-secreting cells and the influence on insulin-responsive target organs. In addition, this paper outlines the clinical applications of extracellular vesicles in insulin resistance. A comprehensive understanding of the regulatory mechanisms and diagnostic status of the inter-organ network in insulin resistance has great potential to advance targeted therapeutic interventions and diagnostic markers, thereby benefiting both the prevention and treatment of insulin resistance.
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Randomized Controlled Trial Comparative Study
Comparison between conventional-dose and high-dose rocuronium use in general anesthesia for Cesarean section.
Background: There have been few studies comparing the effects of high- and low-dose rocuronium during cesarean section by directly measuring the concentration. Therefore, we conducted a study to examine the blood concentrations and clinical effects of both doses of rocuronium on mothers and fetuses. Methods: Eighteen patients were randomly assigned to two groups: C Group (0.6 mg/kg), and H Group, (1.0 mg/kg). ⋯ Rocuronium concentrations in the umbilical vein (p=0.004) and maternal vein before cord clamping (p=0.002) and at discharge (p<0.001) were also found to be higher in the H group than in the C group. Conclusions: We observed no prolongation of PACU stay, and no differences in Apgar scores in H group compared to C group. It suggests that 1.0 mg/kg of rocuronium has no negative effects on the fetus and mother in cesarean section.
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Pulmonary arterial hypertension (PAH) is a severe pulmonary vascular disease characterized by increased pulmonary vascular resistance because of vascular remodeling and vasoconstriction. Subsequently, PAH leads to right ventricular hypertrophy and heart failure. Cell death mechanisms play a significant role in development and tissue homeostasis, and regulate the balance between cell proliferation and differentiation. ⋯ This review summarizes the role of these cell death mechanisms, associated signaling pathways, unique effector molecules, and various pro-survival or reprogramming mechanisms. The aim of this review is to summarize the currently known molecular mechanisms underlying PAH. Further investigations of the cell death mechanisms may unravel new avenues for the prevention and treatment of PAH.
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Hypoxic injury is a critical pathological factor in the development of various cardiovascular diseases, such as congenital heart disease, myocardial infarction, and heart failure. Mitochondrial quality control is essential for protecting cardiomyocytes from hypoxic damage. ⋯ Targeted interventions to enhance mitochondrial quality control, such as coenzyme Q10 and statins, have shown promise in mitigating hypoxia-induced mitochondrial dysfunction. These treatments offer potential therapeutic strategies for hypoxia-related cardiovascular diseases by regulating mitochondrial fission and fusion, restoring mitochondrial biogenesis, reducing ROS production, and promoting mitophagy.