Cardioprotective Effects of Adiponectin-Stimulated Autophagy.

Cardiovascular diseases (CVDs), including heart failure, pose a significant economic and health burden worldwide. Current treatment strategies for heart failure are greatly limited, in that they mainly mitigate symptoms or delay further progression. In contrast, therapies aimed at proactively preventing the onset of heart failure could greatly improve outcomes.

Autophagy deficiency exacerbated hypoxia-reoxygenation induced inflammation and cell death via a mitochondrial DNA/STING/IRF3 pathway.

Aims: Autophagy is an important cellular process for maintaining physiological homeostasis and is known to protect against cardiovascular diseases including ischemia reperfusion (I/R) injury. The underlying mechanisms behind its protection require further characterization.

Materials And Methods: Atg7 knock out (AKO) mice were generated and subjected to I/R injury, complemented by Atg7 KO in a H9c2 cardiomyoblast cellular model ± hypoxia-reoxygenation.

MitoNEET preserves muscle insulin sensitivity during iron overload by regulating mitochondrial iron, reactive oxygen species and fission.

Iron overload (IO) is known to contribute to metabolic dysfunctions such as type 2 diabetes and insulin resistance. Using L6 skeletal muscle cells overexpressing the CDGSH iron-sulfur domain-containing protein 1 (CISD1, also known as mitoNEET) (mitoN) protein, we examined the potential role of MitoN in preventing IO-induced insulin resistance. In L6 control cells, IO resulted in insulin resistance which could be prevented by MitoN as demonstrated by western blot of p-Akt and Akt biosensor cells.

MitoNEET Provides Cardioprotection via Reducing Oxidative Damage and Conserving Mitochondrial Function.

Cardiometabolic diseases exert a significant health impact, leading to a considerable economic burden globally. The metabolic syndrome, characterized by a well-defined cluster of clinical parameters, is closely linked to an elevated risk of cardiovascular disease. Current treatment strategies often focus on addressing individual aspects of metabolic syndrome.

MitoNEET prevents iron overload-induced insulin resistance in H9c2 cells through regulation of mitochondrial iron.

Iron overload (IO) induces insulin resistance in H9c2 cardiomyoblast cells. Here, we used H9c2 cells overexpressing MitoNEET to examine the potential for protection against iron accumulation in the mitochondria and subsequent insulin resistance. In control H9c2 cells, IO was observed to increase mitochondrial iron content, reactive oxygen species (ROS) production, mitochondrial fission, and reduced insulin-stimulated Akt and ERK1/2 phosphorylation.

Role of Mitochondrial Iron Overload in Mediating Cell Death in H9c2 Cells.

Iron overload (IO) is associated with cardiovascular diseases, including heart failure. Our study's aim was to examine the mechanism by which IO triggers cell death in H9c2 cells. IO caused accumulation of intracellular and mitochondrial iron as shown by the use of iron-binding fluorescent reporters, FerroOrange and MitoFerroFluor.

Importance of Autophagy in Mediating Cellular Responses to Iron Overload in Cardiomyocytes.

Both iron overload and deficiency can promote development of cardiomyopathy. Advances in our knowledge from recent research have indicated numerous potential cellular mechanisms. Regulation of myocardial autophagy by iron is of particular interest and will be reviewed here.

Surgical treatment of a Morgagni hernia causing intermittent gastric outlet obstruction.

A Morgagni hernia is a rare diaphragmatic hernia which develops through a congenital defect in the retrosternal area, usually on the right hand side. Because of its congenital aetiology, Morgagni hernias are rarely considered in the differential diagnosis of gastric outlet obstruction symptoms in adults. We present a patient with an incarcerated Morgagni hernia who presented with gastric outlet obstruction.