Exogenous Functional Mitochondria Derived from Bone Mesenchymal Stem Cells That Respond to ROS Can Rescue Neural Cells Following Ischemic Stroke.

Background: Upon uptake by stressed cells, functional mitochondria can perform their normal functions, ultimately enhancing the survival of host cells. However, despite the promising results of this approach, there is still a lack of understanding of the specific relationship between nerve cells and functional mitochondria.

Methods: Functional mitochondria (F-Mito) were isolated from bone marrow-derived mesenchymal stem cells (BMSCs).

SIRT3 alleviates sepsis-induced acute lung injury by inhibiting pyroptosis via regulating the deacetylation of FoxO3a.

Objective: This study mainly analyzes the mechanism of SIRT3 alleviating sepsis-induced acute lung injury (ALI) by regulating the deacetylation of FoxO3a and inhibiting pyroptosis.

Methods: SIRT3-overexpressing and silenced BEAS-2B cells were used to evaluate the effect of SIRT3 on apoptosis in LPS-treated lung epithelial cells. FoxO3a-silenced BEAS-2B cells were also used to verify the mechanism by which SIRT3 inhibited oxidative stress and pyroptosis in vitro in ALI.

Effects of β-blockers therapy on the 28-day and 3-year survival rates of end-stage renal disease patients with cardiovascular disease: a retrospective cohort study.

Background: β-blockers have been used in the treatment of end-stage renal disease (ESRD) patients and cardiovascular disease (CVD) patients, separately. However, the effects of β-blockers on ESRD patients with CVD have not been fully investigated. This study sought to investigate the effects of β-blockers therapy on the 28-day and 3-year survival rates of ESRD patients with pre-existing CVD who were admitted to the intensive care unit (ICU).

Downregulation of tripartite motif protein 11 attenuates cardiomyocyte apoptosis after ischemia/reperfusion injury via DUSP1-JNK1/2.

Currently, the prevention of ischemic diseases such as myocardial infarction associated with ischemia/reperfusion (I/R) injury remains to be a challenge. Thus, this study was designed to explore the effects of tripartite motif protein 11 (TRIM11) on cardiomyocytes I/R injury and its underlying mechanism. Cardiomyocytes AC16 were used to establish an I/R injury cell model.