Autophagy and inflammation in ischemic stroke

Mo, Yufei; Sun, Yinyi; Liu, Kangyong

doi:10.4103/1673-5374.274331

Cited by 236 publications

(43 citation statements)

References 100 publications

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“…Ischemic stroke produces ROS and induces oxidative stress. In response to stress, autophagy exerts a two-way effect in ischemic stroke, and cerebral ischemic injury can be reduced by regulating autophagy (Mo et al, 2020). By enhancing autophagosome formation and promoting fusion of autophagosomes or attenuating autophagic-lysosomal defects, the autophagy-lysosome pathway exerts a protective effect on cerebral ischemia; however, promoting lysosomal dysfunction and autophagic defect exerts a detrimental effect (Chen et al, 2020).…”

Section: Strokementioning

confidence: 99%

Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases

Deng

Liu

et al. 2020

Front. Cell Dev. Biol.

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Autophagy has dual effects in human diseases: appropriate autophagy may protect cells from stress, while excessive autophagy may cause cell death. Additionally, close interactions exist between autophagy and the Golgi. This review outlines recent advances regarding the role of the Golgi apparatus in autophagy. The signaling processes of autophagy are dependent on the normal function of the Golgi. Specifically, (i) autophagy-related protein 9 is mainly located in the Golgi and forms new autophagosomes in response to stressors; (ii) Golgi fragmentation is induced by Golgirelated proteins and accompanied with autophagy induction; and (iii) the endoplasmic reticulum-Golgi intermediate compartment and the reticular trans-Golgi network play essential roles in autophagosome formation to provide a template for lipidation of microtubule-associated protein 1A/1B-light chain 3 and induce further ubiquitination. Golgi-related proteins regulate formation of autophagosomes, and disrupted formation of autophagy can influence Golgi function. Notably, aberrant autophagy has been demonstrated to be implicated in neurological diseases. Thus, targeted therapies aimed at protecting the Golgi or regulating Golgi proteins might prevent or ameliorate autophagy-related neurological diseases. Further studies are needed to investigate the potential application of Golgi therapy in autophagy-based neurological diseases.

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Section: Strokementioning

confidence: 99%

Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases

Deng

Liu

et al. 2020

Front. Cell Dev. Biol.

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“…Activated HIF-1 promotes the expression of BINP3 under ischemic conditions. BNIP3/BNIP3L competes with Beclin 1 and dissociates it from the Beclin 1/Bcl-2 complex, stimulating Beclin 1 to participate in the formation of the autophagosome [ 36 ]. Lu et al demonstrated that hypoxic preconditioning (HPC) activated autophagy through the HIF-1/BNIP3/Beclin 1 signaling pathway in SH-SY5Y cells after oxygen and glucose deprivation/reoxygenation (OGD/R).…”

Section: Signaling Pathways Of Autophagy In Strokementioning

confidence: 99%

Detrimental and Beneficial Effect of Autophagy and a Potential Therapeutic Target after Ischemic Stroke

Wang

Lee

Elkin

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Autophagy, a physiologic mechanism that promotes energy recycling and orderly degradation through self-regulated disassembly of cellular components, helps maintain homeostasis. A series of evidences suggest that autophagy is activated as a response to ischemia and has been well-characterized as a therapeutic target. However, the role of autophagy after ischemia remains controversial. Activated-autophagy can remove necrotic substances against ischemic injury to promote cell survival. On the contrary, activation of autophagy may further aggravate ischemic injury, causing cell death. Therefore, the present review will examine the current understanding of the precise mechanism and role of autophagy in ischemia and recent neuroprotective therapies on autophagy, drug, and nondrug therapies, including electroacupuncture (EA).

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“…Nevertheless, it was proposed that the dysregulation of autophagy in microglia also affects innate immune functions such as phagocytosis and inflammation, which, in turn, contribute to the pathophysiology of aging and neurodegenerative diseases [129]. In neurons, the autophagic-lysosomal pathway plays an important role in the clearance of protein aggregates caused by ischemia-induced neuronal endoplasmic-reticulum stress [130]. It has been suggested that moderate activation of autophagy may prevent neuronal damage to a certain extent, whereas excessive autophagy may be a contributing factor in neuronal death in cerebral ischemia and hypoxia.…”

Section: Autophagy Regulationmentioning

confidence: 99%

Lysosomotropic Features and Autophagy Modulators among Medical Drugs: Evaluation of Their Role in Pathologies

2020

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The concept of lysosomotropic agents significantly changed numerous aspects of cellular biochemistry, biochemical pharmacology, and clinical medicine. In the present review, we focused on numerous low-molecular and high-molecular lipophilic basic compounds and on the role of lipophagy and autophagy in experimental and clinical medicine. Attention was primarily focused on the most promising agents acting as autophagy inducers, which offer a new window for treatment and/or prophylaxis of various diseases, including type 2 diabetes mellitus, Parkinson’s disease, and atherosclerosis. The present review summarizes current knowledge on the lysosomotropic features of medical drugs, as well as autophagy inducers, and their role in pathological processes.

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Autophagy and inflammation in ischemic stroke

Cited by 236 publications

References 100 publications

Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases

Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases

Detrimental and Beneficial Effect of Autophagy and a Potential Therapeutic Target after Ischemic Stroke

Lysosomotropic Features and Autophagy Modulators among Medical Drugs: Evaluation of Their Role in Pathologies

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