Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae.However,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke subtypes.Re...Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae.However,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke subtypes.Recent studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral hemorrhage.Mitophagy,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria.Mitophagy markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral hemorrhage.This review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral hemorrhage.In conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.展开更多
Intracerebral hemorrhage is often accompanied by oxidative stress induced by reactive oxygen species,which causes abnormal mitochondrial function and secondary reactive oxygen species generation.This creates a vicious...Intracerebral hemorrhage is often accompanied by oxidative stress induced by reactive oxygen species,which causes abnormal mitochondrial function and secondary reactive oxygen species generation.This creates a vicious cycle leading to reactive oxygen species accumulation,resulting in progression of the pathological process.Therefore,breaking the cycle to inhibit reactive oxygen species accumulation is critical for reducing neuronal death after intracerebral hemorrhage.Our previous study found that increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4(NADPH oxidase 4,NOX4)led to neuronal apoptosis and damage to the blood-brain barrier after intracerebral hemorrhage.The purpose of this study was to investigate the role of NOX4 in the circle involving the neuronal tolerance to oxidative stress,mitochondrial reactive oxygen species and modes of neuronal death other than apoptosis after intracerebral hemorrhage.We found that NOX4 knockdown by adeno-associated virus(AAV-NOX4)in rats enhanced neuronal tolerance to oxidative stress,enabling them to better resist the oxidative stress caused by intracerebral hemorrhage.Knockdown of NOX4 also reduced the production of reactive oxygen species in the mitochondria,relieved mitochondrial damage,prevented secondary reactive oxygen species accumulation,reduced neuronal pyroptosis and contributed to relieving secondary brain injury after intracerebral hemorrhage in rats.Finally,we used a mitochondria-targeted superoxide dismutase mimetic to explore the relationship between reactive oxygen species and NOX4.The mitochondria-targeted superoxide dismutase mimetic inhibited the expression of NOX4 and neuronal pyroptosis,which is similar to the effect of AAV-NOX4.This indicates that NOX4 is likely to be an important target for inhibiting mitochondrial reactive oxygen species production,and NOX4 inhibitors can be used to alleviate oxidative stress response induced by intracerebral hemorrhage.展开更多
Diffusion tensor tractography allows the sensory fiber course of the medial lemniscus to be visualized. But diffusion tensor tractography for accurate evaluation of the repair of injured somatosensory tracts in stroke...Diffusion tensor tractography allows the sensory fiber course of the medial lemniscus to be visualized. But diffusion tensor tractography for accurate evaluation of the repair of injured somatosensory tracts in stroke patients has been rarely reported. A 55-year-old female patient presented with severe somatosensory dysfunction of the left side caused by a spontaneous intracerebral hemorrhage on the right side. The somatosensory function of the affected side recovered to a nearly normal state at 7 weeks from onset. Functional magnetic resonance imaging revealed that at 3 weeks from onset, there was no cortical activation by touch at each hand; at 7 weeks, the contralateral cortex centered on the primary sensory cortex was found to be activated during touch and passive movements, and activation by passive movements was increased compared with that at 3 weeks. Diffusion tensor tractography revealed that a medial lemniscus on the affected （right） hemisphere was not observed at 3 weeks from onset, however, at 7 weeks, the unaffected （left） hemisphere passed along the medial lemniscus pathway from the pons to the primary sensory cortex. These findings indicate that combined functional magnetic resonance imaging and diffusion tensor tractography would allow more accurate evaluation of the architecture and integrity of somatosensory tracts and is a useful method to investigate the recovery of somatosensory dysfunction in stroke patients.展开更多
BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B...BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B protein and the severity of brain damage.METHODS:This article is a critical and descriptive review on S100 B protein in serum after ischemic brain injury.We searched Pubmed database with key words or terms such as "S100B protein", "cardiac arrest", "hemorrhagic shock" and "ischemia reperfusion injury" appeared in the last five years.RESULTS:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of ischemic brain injury will be dramatically increased.Ischemic brain injury elevated the level of serum S100 B protein,and the severity of brain damage.CONCLUSION:The level of S100 B protein in serum is elevated after ischemic brain injury,but its mechanism is unclear.展开更多
BACKGROUND： Conventional neuroimaging diagnosis does not assist with the monitoring or evaluation of basal nuclei ischemic and hemorrhagic stroke, or motor functional recovery. Magnetic resonance, diffusion tensor im...BACKGROUND： Conventional neuroimaging diagnosis does not assist with the monitoring or evaluation of basal nuclei ischemic and hemorrhagic stroke, or motor functional recovery. Magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography have all been used to observe features of cerebral white matter fibrous structures. In addition, diffusion tensor tractography is the only non-invasive imaging method to display the corticospinal tract in vivo. OBJECTIVE： To evaluate the impairment degree of corticospinal tract induced by basal nuclei ischemic and hemorrhagic stroke through the use of magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography, and to analyze the correlation to muscular strength. DESIGN, TIME AND SETTING： A retrospective case analysis was performed at the Department of Medical Imaging, Neurology and Neurosurgery, Fuzhou General Hospital of Nanjing Military Area Command of Chinese PLA between November 2002 and June 2008. PARTICIPANTS： A total of 15 patients with acute or subacute cerebral ischemic stroke and nine with hemorrhagic stroke in the basal nuclei were selected. METHODS： Magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography results and data were analyzed. Fractional anisotropy and directionally encoded color maps were obtained. Three-dimensional tractography of bilateral corticospinal tract was created, and corticospinal tract integrity was graded. Fractional anisotropy of infarct region and corresponding contralateral normal regions were measured, and hematoma volume in hemorrhagic stroke patients was determined. Hand motor function ability was evaluated using Brunstorm criteria. MAIN OUTCOME MEASURES： Fractional anisotropy of infarct region and corresponding contralateral normal regions; hematoma volume in hemorrhagic stroke patients; correlation between muscular strength and corticospinal tract impairment degree in ischemic stroke and hemorrhagic stroke patients before and after treatment. RESULTS： In ischemic stroke patients, the fractional anisotropy value was significantly lower in the infarct area of white matter than in the normal hemisphere （P 〈 0.01）. The impairment degree of corticospinal tract negatively correlated with muscular strength of the corresponding hand （r = -0.97 P 〈 0.01）. The hematoma volume of hemorrhagic stroke patients significantly negatively correlated with Spearman test results for muscular strength of the corresponding hand （r = -0.88, P 〈 0.01）. CONCLUSION： Corticospinal tract impairment severity negatively correlated with muscular strength and motor functional recovery, which suggested that diffusion tensor imaging and diffusion tensor tractography could be used to evaluate corticospinal tract motor function.展开更多
Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal apoptosis.OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive...Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal apoptosis.OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke.Therefore,OLR1 is likely involved in the progress of intracerebral hemorrhage.In this study,we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model.OLR1 small interfering RNA(10μL;50 pmol/μL)was injected into the right basal ganglia to knock down OLR1.Twenty-four hours later,0.5 U collagenase type VII was injected to induce intracerebral hemorrhage.We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma,neuron loss,inflammatory reaction,and oxidative stress in rat brain tissue.We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway.Therefore,silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage.These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.展开更多
The aberrant pyramidal tract is the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem. A 21-year-old man presented with right hemiparesis due to a traumatic intracerebral hemorrha...The aberrant pyramidal tract is the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem. A 21-year-old man presented with right hemiparesis due to a traumatic intracerebral hemorrhage in the left corona radiata. His motor function recovered almost to the normal state at 10 months after onset. Through diffusion tensor tractography, the pyramidal tract in the affected （left） hemisphere showed discontinuation at the pontine level at 13 months after onset. An aberrant pyramidal tract was observed, which originated from the primary motor cortex and the supplementary motor area and descended through the corona radiata, then through the posterior limb of the internal capsule and the medial lemniscus pathway from the midbrain to the pons, finally entered into the pyramidal tract area at the pontomedullary junction, it suggests that the motor functions of the right extremities in this patient had recovered by this aberrant pyramidal tract.展开更多
Clinical advances in the treatment of intracranial hemorrhage(ICH)are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury.Acrolein is a highly active unsaturat...Clinical advances in the treatment of intracranial hemorrhage(ICH)are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury.Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases.Our results indicated a significant increase in the level of acrolein after ICH in mouse brain.In primary neurons,acrolein induced an increase in mitochondrial fragmentation,loss of mitochondrial membrane potential,generation of reactive oxidative species,and release of mitochondrial cytochrome c.Mechanistically,acrolein facilitated the translocation of dynaminrelated protein 1(Drpl)from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission.Further studies found that treatment with hydralazine(an acrolein scavenger)significantly reversed Drpl translocation and the morphological damage of mitochondria after ICH.In parallel,the neural apoptosis,brain edema,and neurological functional deficits induced by ICH were also remarkably alleviated.In conclusion,our results identify acrolein as an important contributor to the secondary brain injury following ICH.Meanwhile,we uncovered a novel mechanism by which Drpl-mediated mitochondrial oxidative damage is involved in acroleininduced brain injury.展开更多
Acute central nervous system injuries,including ischemic stro ke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal co rd injury,are a major global health challenge.Identifying optimal ...Acute central nervous system injuries,including ischemic stro ke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal co rd injury,are a major global health challenge.Identifying optimal therapies and improving the long-term neurological functions of patients with acute central nervous system injuries are urgent priorities.Mitochondria are susceptible to damage after acute central nervous system injury,and this leads to the release of toxic levels of reactive oxygen species,which induce cell death.Mitophagy,a selective form of autophagy,is crucial in eliminating redundant or damaged mitochondria during these events.Recent evidence has highlighted the significant role of mitophagy in acute central nervous system injuries.In this review,we provide a comprehensive overview of the process,classification,and related mechanisms of mitophagy.We also highlight the recent developments in research into the role of mitophagy in various acute central nervous system injuries and drug therapies that regulate mitophagy.In the final section of this review,we emphasize the potential for treating these disorders by focusing on mitophagy and suggest future research paths in this area.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82071382(to MZ),81601306(to HS)The Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)(to MZ)+5 种基金Jiangsu 333 High-Level Talent Training Project(2022)(to HS)The Jiangsu Maternal and Child Health Research Key Project,No.F202013(to HS)Jiangsu Talent Youth Medical Program,No.QNRC2016245(to HS)Shanghai Key Lab of Forensic Medicine,No.KF2102(to MZ)Suzhou Science and Technology Development Project,No.SYS2020089(to MZ)The Fifth Batch of Gusu District Health Talent Training Project,No.GSWS2019060(to HS)。
文摘Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae.However,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke subtypes.Recent studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral hemorrhage.Mitophagy,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria.Mitophagy markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral hemorrhage.This review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral hemorrhage.In conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.
基金supported by the National Natural Science Foundation of China,No.81671125the Natural Science Foundation of Guangdong Province,No.2021A1515011115Guangzhou Science and Technology Project,No.202102010346(all to YZC)。
文摘Intracerebral hemorrhage is often accompanied by oxidative stress induced by reactive oxygen species,which causes abnormal mitochondrial function and secondary reactive oxygen species generation.This creates a vicious cycle leading to reactive oxygen species accumulation,resulting in progression of the pathological process.Therefore,breaking the cycle to inhibit reactive oxygen species accumulation is critical for reducing neuronal death after intracerebral hemorrhage.Our previous study found that increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4(NADPH oxidase 4,NOX4)led to neuronal apoptosis and damage to the blood-brain barrier after intracerebral hemorrhage.The purpose of this study was to investigate the role of NOX4 in the circle involving the neuronal tolerance to oxidative stress,mitochondrial reactive oxygen species and modes of neuronal death other than apoptosis after intracerebral hemorrhage.We found that NOX4 knockdown by adeno-associated virus(AAV-NOX4)in rats enhanced neuronal tolerance to oxidative stress,enabling them to better resist the oxidative stress caused by intracerebral hemorrhage.Knockdown of NOX4 also reduced the production of reactive oxygen species in the mitochondria,relieved mitochondrial damage,prevented secondary reactive oxygen species accumulation,reduced neuronal pyroptosis and contributed to relieving secondary brain injury after intracerebral hemorrhage in rats.Finally,we used a mitochondria-targeted superoxide dismutase mimetic to explore the relationship between reactive oxygen species and NOX4.The mitochondria-targeted superoxide dismutase mimetic inhibited the expression of NOX4 and neuronal pyroptosis,which is similar to the effect of AAV-NOX4.This indicates that NOX4 is likely to be an important target for inhibiting mitochondrial reactive oxygen species production,and NOX4 inhibitors can be used to alleviate oxidative stress response induced by intracerebral hemorrhage.
基金the National Research Foundation of Korea Grant Funded by the Korean Government,No.KRF-2008-314-E00173
文摘Diffusion tensor tractography allows the sensory fiber course of the medial lemniscus to be visualized. But diffusion tensor tractography for accurate evaluation of the repair of injured somatosensory tracts in stroke patients has been rarely reported. A 55-year-old female patient presented with severe somatosensory dysfunction of the left side caused by a spontaneous intracerebral hemorrhage on the right side. The somatosensory function of the affected side recovered to a nearly normal state at 7 weeks from onset. Functional magnetic resonance imaging revealed that at 3 weeks from onset, there was no cortical activation by touch at each hand; at 7 weeks, the contralateral cortex centered on the primary sensory cortex was found to be activated during touch and passive movements, and activation by passive movements was increased compared with that at 3 weeks. Diffusion tensor tractography revealed that a medial lemniscus on the affected （right） hemisphere was not observed at 3 weeks from onset, however, at 7 weeks, the unaffected （left） hemisphere passed along the medial lemniscus pathway from the pons to the primary sensory cortex. These findings indicate that combined functional magnetic resonance imaging and diffusion tensor tractography would allow more accurate evaluation of the architecture and integrity of somatosensory tracts and is a useful method to investigate the recovery of somatosensory dysfunction in stroke patients.
基金supported by a grant from 122 Project of Nanjing Military Command focusing on training(JQZD200905)
文摘BACKGROUND:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of global cerebral ischemic injury will be dramatically increased.Ischemic brain injury may elevate the level of serum S100 B protein and the severity of brain damage.METHODS:This article is a critical and descriptive review on S100 B protein in serum after ischemic brain injury.We searched Pubmed database with key words or terms such as "S100B protein", "cardiac arrest", "hemorrhagic shock" and "ischemia reperfusion injury" appeared in the last five years.RESULTS:S100B protein in patients with cardiac arrest,hemorrhagic shock and other causes of ischemic brain injury will be dramatically increased.Ischemic brain injury elevated the level of serum S100 B protein,and the severity of brain damage.CONCLUSION:The level of S100 B protein in serum is elevated after ischemic brain injury,but its mechanism is unclear.
基金a Grant from the Science and Technology Department of Fujian Province,No.2006J0192
文摘BACKGROUND： Conventional neuroimaging diagnosis does not assist with the monitoring or evaluation of basal nuclei ischemic and hemorrhagic stroke, or motor functional recovery. Magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography have all been used to observe features of cerebral white matter fibrous structures. In addition, diffusion tensor tractography is the only non-invasive imaging method to display the corticospinal tract in vivo. OBJECTIVE： To evaluate the impairment degree of corticospinal tract induced by basal nuclei ischemic and hemorrhagic stroke through the use of magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography, and to analyze the correlation to muscular strength. DESIGN, TIME AND SETTING： A retrospective case analysis was performed at the Department of Medical Imaging, Neurology and Neurosurgery, Fuzhou General Hospital of Nanjing Military Area Command of Chinese PLA between November 2002 and June 2008. PARTICIPANTS： A total of 15 patients with acute or subacute cerebral ischemic stroke and nine with hemorrhagic stroke in the basal nuclei were selected. METHODS： Magnetic resonance, diffusion tensor imaging, and diffusion tensor tractography results and data were analyzed. Fractional anisotropy and directionally encoded color maps were obtained. Three-dimensional tractography of bilateral corticospinal tract was created, and corticospinal tract integrity was graded. Fractional anisotropy of infarct region and corresponding contralateral normal regions were measured, and hematoma volume in hemorrhagic stroke patients was determined. Hand motor function ability was evaluated using Brunstorm criteria. MAIN OUTCOME MEASURES： Fractional anisotropy of infarct region and corresponding contralateral normal regions; hematoma volume in hemorrhagic stroke patients; correlation between muscular strength and corticospinal tract impairment degree in ischemic stroke and hemorrhagic stroke patients before and after treatment. RESULTS： In ischemic stroke patients, the fractional anisotropy value was significantly lower in the infarct area of white matter than in the normal hemisphere （P 〈 0.01）. The impairment degree of corticospinal tract negatively correlated with muscular strength of the corresponding hand （r = -0.97 P 〈 0.01）. The hematoma volume of hemorrhagic stroke patients significantly negatively correlated with Spearman test results for muscular strength of the corresponding hand （r = -0.88, P 〈 0.01）. CONCLUSION： Corticospinal tract impairment severity negatively correlated with muscular strength and motor functional recovery, which suggested that diffusion tensor imaging and diffusion tensor tractography could be used to evaluate corticospinal tract motor function.
基金supported by the National Natural Science Foundation of China,No.81971125(to ZYH).
文摘Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal apoptosis.OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke.Therefore,OLR1 is likely involved in the progress of intracerebral hemorrhage.In this study,we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model.OLR1 small interfering RNA(10μL;50 pmol/μL)was injected into the right basal ganglia to knock down OLR1.Twenty-four hours later,0.5 U collagenase type VII was injected to induce intracerebral hemorrhage.We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma,neuron loss,inflammatory reaction,and oxidative stress in rat brain tissue.We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway.Therefore,silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage.These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.
基金supported by Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education,Science and Technology,No.2012R1A1A4A01001873
文摘The aberrant pyramidal tract is the collateral pathway of the pyramidal tract through the medial lemniscus in the brainstem. A 21-year-old man presented with right hemiparesis due to a traumatic intracerebral hemorrhage in the left corona radiata. His motor function recovered almost to the normal state at 10 months after onset. Through diffusion tensor tractography, the pyramidal tract in the affected （left） hemisphere showed discontinuation at the pontine level at 13 months after onset. An aberrant pyramidal tract was observed, which originated from the primary motor cortex and the supplementary motor area and descended through the corona radiata, then through the posterior limb of the internal capsule and the medial lemniscus pathway from the midbrain to the pons, finally entered into the pyramidal tract area at the pontomedullary junction, it suggests that the motor functions of the right extremities in this patient had recovered by this aberrant pyramidal tract.
基金This work was supported by grants from the National Natural Science Foundation of China(81630027,81571215)and the Chang Jiang Scholar Program of China.
文摘Clinical advances in the treatment of intracranial hemorrhage(ICH)are restricted by the incomplete understanding of the molecular mechanisms contributing to secondary brain injury.Acrolein is a highly active unsaturated aldehyde which has been implicated in many nervous system diseases.Our results indicated a significant increase in the level of acrolein after ICH in mouse brain.In primary neurons,acrolein induced an increase in mitochondrial fragmentation,loss of mitochondrial membrane potential,generation of reactive oxidative species,and release of mitochondrial cytochrome c.Mechanistically,acrolein facilitated the translocation of dynaminrelated protein 1(Drpl)from the cytoplasm onto the mitochondrial membrane and led to excessive mitochondrial fission.Further studies found that treatment with hydralazine(an acrolein scavenger)significantly reversed Drpl translocation and the morphological damage of mitochondria after ICH.In parallel,the neural apoptosis,brain edema,and neurological functional deficits induced by ICH were also remarkably alleviated.In conclusion,our results identify acrolein as an important contributor to the secondary brain injury following ICH.Meanwhile,we uncovered a novel mechanism by which Drpl-mediated mitochondrial oxidative damage is involved in acroleininduced brain injury.
基金supported by the National Natural Science Foundation of China,Nos.81920108017(to YX),82130036(to YX),82371326(to XC),82171310(to XC)the STI2030-Major Projects,No.2022ZD0211800(to YX)Jiangsu Province Key Medical Discipline,No.ZDXK202216(to YX)。
文摘Acute central nervous system injuries,including ischemic stro ke,intracerebral hemorrhage,subarachnoid hemorrhage,traumatic brain injury,and spinal co rd injury,are a major global health challenge.Identifying optimal therapies and improving the long-term neurological functions of patients with acute central nervous system injuries are urgent priorities.Mitochondria are susceptible to damage after acute central nervous system injury,and this leads to the release of toxic levels of reactive oxygen species,which induce cell death.Mitophagy,a selective form of autophagy,is crucial in eliminating redundant or damaged mitochondria during these events.Recent evidence has highlighted the significant role of mitophagy in acute central nervous system injuries.In this review,we provide a comprehensive overview of the process,classification,and related mechanisms of mitophagy.We also highlight the recent developments in research into the role of mitophagy in various acute central nervous system injuries and drug therapies that regulate mitophagy.In the final section of this review,we emphasize the potential for treating these disorders by focusing on mitophagy and suggest future research paths in this area.
