Inhibition of the cGAS–STING pathway:contributing to the treatment of cerebral ischemia-reperfusion injury

The cGAS–STING pathway plays an important role in ischemia-reperfusion injury in the heart,liver,brain,and kidney,but its role and mechanisms in cerebral ischemia-reperfusion injury have not been systematically reviewed.Here,we outline the components of the cGAS–STING pathway and then analyze its role in autophagy,ferroptosis,cellular pyroptosis,disequilibrium of calcium homeostasis,inflammatory responses,disruption of the blood–brain barrier,microglia transformation,and complement system activation following cerebral ischemia-reperfusion injury.We further analyze the value of cGAS–STING pathway inhibitors in the treatment of cerebral ischemia-reperfusion injury and conclude that the pathway can regulate cerebral ischemia-reperfusion injury through multiple mechanisms.Inhibition of the cGAS–STING pathway may be helpful in the treatment of cerebral ischemia-reperfusion injury.

The main causes and corresponding solutions of skin pigmentation in the body

The skin's normal color is primarily determined by the quantity and distribution of pigment,the level of hemoglobin in the skin's blood vessels,and various optical factors.Additionally,mechanical damage from clothing renders certain areas of the body more susceptible to hyperpigmentation,such as the elbows and knees.According to research,various factors such as gender and weight have been found to influence skin color.The mechanism of body skin pigmentation has been extensively studied with a particular focus on melanogenesis and related signaling pathways.Therefore,this article primarily focuses on elucidating the mechanisms governing body pigmentation while discussing strategies for managing skin whitening,encompassing influential factors and whitening methods.

Endogenous/exogenous dual stimulation“ROS engineering”amplification combined with autophagy-augmented for efficient ferroptosis therapy

“Reactive oxygen species(ROS)engineering”is one of the most promising anti-tumor treatments developed in recent years.Massive explosion of ROS will cause oxidative stress,thereby inducing tumor cell death.However,ROS accumulation in tumor cells is eliminated by endogenous cellular self-regulation strategies.In this work,a kind of endogenous/exogenous dual stimulation nanoagent noted as UMZC is developed.Fenton reaction occurs between NH_(2)-MIL-88B(Fe)contained in UMZC and the overexpression of endogenous H_(2)O_(2)to generate ROS,amplified by endogenous H_(2)S of colon tumor cells.In addition,NH_(2)-MIL-88B(Fe)also functions to deplete glutathione(GSH)for stopping it from consuming ROS.Upconversion nanoparticles at the core of UMZC convert near-infrared into visible light,which excites zinc phthalocyanine to initiate the photochemical reaction that generates more ROS,thus alleviating the lack of tissue penetration depth for visible light.Autophagy agonist chitosan oligosaccharides induce enhancement of cellular autophagy for disrupting cellular metabolic stress and the resistance to oxidative stress of tumor cells,allowing“ROS engineering”to fully exert anti-tumor effects.All of ROS generation,GSH depletion,and induced cellular autophagy caused by nanoagents have promoting effects on the occurrence of ferroptosis.Finally,the nanoagents show the ability to effectively treat colon tumors.