Research progress on astrocyte autophagy in ischemic stroke

Su, Pei-Wei; Zhai, Zhe; Wang, Tong; Zhang, Yanan; Wang, Yuan; Ma, Ke; Han, Bing-Bing; Wu, Zhi-Chun; Yu, Hua-Yun; Zhao, Haijun; Wang, Shijun

doi:10.3389/fneur.2022.951536

Cited by 6 publications

(5 citation statements)

References 142 publications

(168 reference statements)

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“…The rat cerebral cortex astrocytes were exposed to peroxide to form an oxidative stress model. After 2 hours of propofol treatment, it was found that the Glu release was significantly lower than that of the untreated group ( 14 , 20 ). Therefore, the combination of O 3 and propofol in this study has a better protective effect on stroke.…”

Section: Discussionmentioning

confidence: 82%

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Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes

Huang¹,

Gao²,

Shi³

et al. 2023

Ann Transl Med

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Background Stroke is a common and damaging disease of brain tissue, and has high morbidity, disability, and mortality rates. Ozone (O 3 ) is an isomer of oxygen and can be applied to ozonate the isolated blood in specific containers outside the body and return it to the body. O 3 can also alter the activity and function of multiple cellular components, thus affecting blood viscosity and altering hemodynamics. However, the question of whether O 3 has clinical value in the treatment of stroke requires further investigation. This study sought to evaluate the protective effect and possible mechanism of O 3 in brain injury after stroke. Methods First, oxygen-glucose deprivation/reoxygenation (OGD/R)-induced human glioblastoma cell (A172) and middle cerebral artery occlusion (MCAO) rat models were established. Second, the levels of the associated ribonucleic acids and proteins were analyzed using reverse-transcription real-time-quantitative polymerase chain reaction, Western Blot, or immunofluorescence assays. Third, the concentration of glutamate and lactate dehydrogenase (LDH) were assessed using enzyme-linked immunoassays. Results The results showed that glial fibrillary acidic protein was upregulated in the OGD/R A172 cells. O 3 decreased LDH and increased glutamate levels in the OGD/R A172 cells, which suggests that O 3 reduced brain damage in the in vitro stroke model. We also showed that O 3 attenuated brain infarction in the in-vivo stroke model. Further, we found that O 3 alleviated stroke-induced brain damage by reducing the apoptosis of astrocytes. Further, the B-cell lymphoma 2 inhibitor propofol alleviated stroke-induced brain damage. Conclusions Thus, O 3 notably alleviated stroke-induced brain damage by inhibiting the apoptosis of astrocytes in the OGD/R-induced human glioblastoma cell and MACO rat models.

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Section: Discussionmentioning

confidence: 82%

“…A study ( 14 ) has reported that autophagy in astrocytes induces the activation of astrocytes, which is common after stroke and causes brain damage. Thus, we speculated that the effect of O 3 in alleviating brain damage might be related to the autophagy of astrocytes.…”

Section: Resultsmentioning

confidence: 99%

Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes

Huang¹,

Gao²,

Shi³

et al. 2023

Ann Transl Med

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“…Astrocytes and neurons exhibit varying degrees of autophagy under hypoxic-ischemic conditions, which may be linked to differences in the mechanisms that activate autophagy. [42]…”

Section: Discussionmentioning

confidence: 99%

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

Shi,

Xu,

et al. 2023

Medicine

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Background: Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process that typically occurs during the treatment of ischemia, with limited therapeutic options. Autophagy plays a vital role during the reperfusion phase and is a potential therapeutic target for preventing and treating cerebral ischemia-reperfusion injury. Methods: We conducted a comprehensive search of the Web of Science Core Collection for publications related to cerebral ischemia-reperfusion injury with autophagy, published between January 1, 2008, and January 1, 2023. We analyzed the selected publications using VOSviewer, CiteSpace, and other bibliometric tools. Results: Our search yielded 877 relevant publications. The field of autophagy in cerebral ischemia-reperfusion injury has grown rapidly since 2016. China has been the leading contributor to publications, followed by the USA and Iran. Chen Zhong and Qin Zhenghong have been influential in this field but have yet to reach all groups. In addition, there has been a shortage of collaboration among authors from different institutions. Our literature and keyword analysis identified Neurovascular protection (#11 Neuroprotective, #13 Neurovascular units, etc) and Inflammation (NLRP3 inflammasome) as popular research directions. Furthermore, the terms “Blood-Brain Barrier,” “Mitophagy,” and “Endoplasmic reticulum stress” have been frequently used and may be hot research topics in the future. Conclusions: The role of autophagy in cerebral ischemia-reperfusion injury remains unclear, and the specific mechanisms of drugs used to treat ischemia-reperfusion injury still need to be explored. This work outlines the changing trends in investigating cerebral ischemia-reperfusion injury involving autophagy and suggests future lines of inquiry.

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“…Autophagy is regulated through the posttranslational modification of ATG proteins, encompassing processes such as phosphorylation, ubiquitination, acetylation, O-GlcNAcylation, N6-methyladenosine modification, oxidation, and cleavage. These modifications serve as indicators that can be monitored to assess the status of the autophagic process [202][203][204][205][206][207][208]. There are many methods for monitoring autophagy, including transmission electron microscopy (TEM), Western blot, immunofluorescence, flow cytometry, northern blot, reverse transcriptase polymerase chain reaction (RT-PCR), luciferase release assay, transgenic mice, and gene knockdown, to identify and quantify the status of autophagic flux in different pathological conditions.…”

Section: Future Research Avenues Monitoring Methods and Unresolved Qu...mentioning

confidence: 99%

The Molecular Mechanism and Therapeutic Application of Autophagy for Urological Disease

Chueh,

Lu,

Juan

et al. 2023

IJMS

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Autophagy is a lysosomal degradation process known as autophagic flux, involving the engulfment of damaged proteins and organelles by double-membrane autophagosomes. It comprises microautophagy, chaperone-mediated autophagy (CMA), and macroautophagy. Macroautophagy consists of three stages: induction, autophagosome formation, and autolysosome formation. Atg8-family proteins are valuable for tracking autophagic structures and have been widely utilized for monitoring autophagy. The conversion of LC3 to its lipidated form, LC3-II, served as an indicator of autophagy. Autophagy is implicated in human pathophysiology, such as neurodegeneration, cancer, and immune disorders. Moreover, autophagy impacts urological diseases, such as interstitial cystitis /bladder pain syndrome (IC/BPS), ketamine-induced ulcerative cystitis (KIC), chemotherapy-induced cystitis (CIC), radiation cystitis (RC), erectile dysfunction (ED), bladder outlet obstruction (BOO), prostate cancer, bladder cancer, renal cancer, testicular cancer, and penile cancer. Autophagy plays a dual role in the management of urologic diseases, and the identification of potential biomarkers associated with autophagy is a crucial step towards a deeper understanding of its role in these diseases. Methods for monitoring autophagy include TEM, Western blot, immunofluorescence, flow cytometry, and genetic tools. Autophagosome and autolysosome structures are discerned via TEM. Western blot, immunofluorescence, northern blot, and RT-PCR assess protein/mRNA levels. Luciferase assay tracks flux; GFP-LC3 transgenic mice aid study. Knockdown methods (miRNA and RNAi) offer insights. This article extensively examines autophagy’s molecular mechanism, pharmacological regulation, and therapeutic application involvement in urological diseases.

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Research progress on astrocyte autophagy in ischemic stroke

Cited by 6 publications

References 142 publications

Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes

Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

The Molecular Mechanism and Therapeutic Application of Autophagy for Urological Disease

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