PINK1 antagonize intracerebral hemorrhage by promoting mitochondrial autophagy

Li, Jingchen; Wu, Xingwang; He, Yuhui; Wu, Song; Guo, Erkun; Feng, Yan; Yang, Jianhui

doi:10.1002/acn3.51425

Cited by 9 publications

(5 citation statements)

References 38 publications

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“…In addition, PTEN-induced kinase 1 (PINK1) is a mitochondrial-targeted protein kinase. By encouraging mitophagy in microglia, PINK1 defends against ICH-induced SBI, and PINK1 overexpression can treat ICH-induced behavioral problems ( Li et al, 2021b ). As a vital component of the mitochondrial contact site and cristae junction organizing system, MIC60 plays a significant role in maintaining the mitochondrial structure and functioning.…”

Section: Dual Role Of Autophagy In Ichmentioning

confidence: 99%

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Lenahan³

et al. 2023

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH) is the second-largest stroke subtype and has a high mortality and disability rate. Secondary brain injury (SBI) is delayed after ICH. The main contributors to SBI are inflammation, oxidative stress, and excitotoxicity. Harmful substances from blood and hemolysis, such as hemoglobin, thrombin, and iron, induce SBI. When cells suffer stress, a critical protective mechanism called “autophagy” help to maintain the homeostasis of damaged cells, remove harmful substances or damaged organelles, and recycle them. Autophagy plays a critical role in the pathology of ICH, and its function remains controversial. Several lines of evidence demonstrate a pro-survival role for autophagy in ICH by facilitating the removal of damaged proteins and organelles. However, many studies have found that heme and iron can aggravate SBI by enhancing autophagy. Autophagy and inflammation are essential culprits in the progression of brain injury. It is a fascinating hypothesis that autophagy regulates inflammation in ICH-induced SBI. Autophagy could degrade and clear pro-IL-1β and apoptosis-associated speck-like protein containing a CARD (ASC) to antagonize NLRP3-mediated inflammation. In addition, mitophagy can remove endogenous activators of inflammasomes, such as reactive oxygen species (ROS), inflammatory components, and cytokines, in damaged mitochondria. However, many studies support the idea that autophagy activates microglia and aggravates microglial inflammation via the toll-like receptor 4 (TLR4) pathway. In addition, autophagy can promote ICH-induced SBI through inflammasome-dependent NLRP6-mediated inflammation. Moreover, some resident cells in the brain are involved in autophagy in regulating inflammation after ICH. Some compounds or therapeutic targets that regulate inflammation by autophagy may represent promising candidates for the treatment of ICH-induced SBI. In conclusion, the mutual regulation of autophagy and inflammation in ICH is worth exploring. The control of inflammation by autophagy will hopefully prove to be an essential treatment target for ICH.

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Section: Dual Role Of Autophagy In Ichmentioning

confidence: 99%

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Lenahan³

et al. 2023

Front. Cell. Neurosci.

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“…Overexpression of PINK1 was able to activate the PINK1-Parkin pathway and rescue IS-induced behavioral disorders. PINK1 protects IS-induced brain injury by promoting mitochondrial autophagy in microglia, which may be of value as a therapeutic target for IS treatment (Li et al, 2021). The mTOR inhibitor rapamycin significantly reduces mTOR activation and infarct volume by activating autophagy and inhibiting neuronal apoptosis, improving neural function after IS (Wu et al, 2018a).…”

Section: Beneficial Role Of Autophagy In Ismentioning

confidence: 99%

New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival

Gao

Wang

Jiang

et al. 2022

Front. Cell Dev. Biol.

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Autophagy is a dynamic process that maintains the normal homeostasis of cells by digesting and degrading aging proteins and damaged organelles. The effect of autophagy on neural tissue is still a matter of debate. Some authors suggest that autophagy has a protective effect on nerve cells, whereas others suggest that autophagy also induces the death of nerve cells and aggravates nerve injury. In mammals, oxidative stress, autophagy and endoplasmic reticulum stress (ERS) constitute important defense mechanisms to help cells adapt to and survive the stress conditions caused by physiological and pathological stimuli. Under many pathophysiological conditions, oxidative stress, autophagy and ERS are integrated and amplified in cells to promote the progress of diseases. Over the past few decades, oxidative stress, autophagy and ERS and their interactions have been a hot topic in biomedical research. In this review, we summarize recent advances in understanding the interactions between oxidative stress, autophagy and ERS in neuronal cell death and survival.

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“…MiRNA-144 has been involved in hemoglobin-mediated microglial autophagic induction and inflammatory response through the mTOR pathway, which exacerbated neurological symptoms and led to brain function impairment after ICH ( Wang et al, 2017 ). Recent studies have found that PINK1, a key enzyme in mitochondria, can promote mitophagy in microglia to protect against ICH-induced brain injury ( Li J. et al, 2021 ). In summary, Microglial autophagy presents a bidirectional role in ICH.…”

Section: Interaction Between Microglial Autophagy and Other Biologica...mentioning

confidence: 99%

Microglial autophagy in cerebrovascular diseases

Chen

Zhang

Chu

et al. 2022

Front. Aging Neurosci.

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Microglia are considered core regulators for monitoring homeostasis in the brain and primary responders to central nervous system (CNS) injuries. Autophagy affects the innate immune functions of microglia. Recently some evidence suggests that microglial autophagy is closely associated with brain function in both ischemic stroke and hemorrhagic stroke. Herein, we will discuss the interaction between autophagy and other biological processes in microglia under physiological and pathological conditions and highlight the interaction between microglial metabolism and autophagy. In the end, we focus on the effect of microglial autophagy in cerebrovascular diseases.

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PINK1 antagonize intracerebral hemorrhage by promoting mitochondrial autophagy

Cited by 9 publications

References 38 publications

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?

New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival

Microglial autophagy in cerebrovascular diseases

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