Autophagy and apoptosis are two important catabolic processes contributing to the maintenance of cellular and tissue homeostasis. Autophagy controls the turnover of protein aggregates and damaged organelles within cells, while apoptosis is the principal mechanism by which unwanted cells are dismantled and eliminated from organisms. Despite marked differences between these two pathways, they are highly interconnected in determining the fate of cells. Intriguingly, caspases, the primary drivers of apoptotic cell death, play a critical role in mediating the complex crosstalk between autophagy and apoptosis. Pro-apoptotic signals can converge to activate caspases to execute apoptotic cell death. In addition, activated caspases can degrade autophagy proteins (i.e., Beclin-1, Atg5, and Atg7) to shut down the autophagic response. Moreover, caspases can convert pro-autophagic proteins into pro-apoptotic proteints to trigger apoptotic cell death instead. It is clear that caspases are important in both apoptosis and autophagy, thus a detailed deciphering of the role of caspases in these two processes is still required to clarify the functional relationship between them. In this article, we provide a current overview of caspases in its interplay between autophagy and apoptosis. We emphasized that defining the role of caspases in autophagy-apoptosis crosstalk will provide a framework for more precise manipulation of these two processes during cell death.

The K(+)-Cl(-) cotransporter-2 (KCC2) is a well-known member of the electroneutral cation-chloride cotransporters with a restricted expression pattern to neurons. This transmembrane protein mediates the efflux of Cl(-) out of neurons and exerts a critical role in inhibitory γ-aminobutyric acidergic (GABAergic) and glycinergic neurotransmission. Moreover, KCC2 participates in the regulation of various physiological processes of neurons, including cell migration, dendritic outgrowth, spine morphology, and dendritic synaptogenesis. It is important to note that down-regulation of KCC2 is associated with the pathogenesis of multiple neurological diseases, which is of particular relevance to acute central nervous system (CNS) injury. In this review, we aim to survey the pathogenic significance of KCC2 down-regulation under the condition of acute CNS injuries. We propose that further elucidation of the molecular mechanisms regarding KCC2 down-regulation after acute CNS injuries is necessary because of potential promising avenues for prevention and treatment of acute CNS injury.

Background: Psychological adaptation after cardiac pacemaker implantation is a challenge for patients with mental illness. Case presentation: Here we report a self-harming patient with a psychiatric disorder. A 73-year-old female patient with 16-year coronary heart disease and a 4-year depression was admitted to our hospital for a coma. Two months earlier, the local hospital confirmed that the patient had a second-degree sinoatrial (SA) block (type 2) as well as basal septal hypertrophy with the left ventricular outflow obstruction. Therefore, metoprolol sustained-release tablets 95 mg QD and diltiazem sustained-release tablets 90 mg QD was given as treatment after a pacemaker was implanted. However, the patient had continued complaining about discomfort due to the pacemaker implanted after being discharged from the hospital. Two months later, she attempted to commit suicide by removing her pacemaker and taking 80 sleeping pills. After a series of treatments, the patient improved and was discharged without a pacemaker re-implantation. With continued anti-depression treatment and strengthen family supervision, the patient's condition is stable now. Conclusions: A suicide attempt by intentionally removing the permanent pacemaker system was rarely reported. In bradycardia patients with a history of psychological or psychiatric disease, careful evaluation should be done before and after implantation of the pacemaker.