Journal
ACTA PHARMACEUTICA SINICA B
Volume 11, Issue 7, Pages 1708-1720Publisher
INST MATERIA MEDICA, CHINESE ACAD MEDICAL SCIENCES
DOI: 10.1016/j.apsb.2020.10.018
Keywords
Autophagy; Cerebral ischemia; Neuroprotection; Mitochondria; Lysosomal activation; Mitophagy; Natural compounds; Neurological disorders
Categories
Funding
- National Natural Science Foundation of China [81822044, 81773703, 81630098]
- Fundamental Research Funds for the Central Universities [2019XZZX004-17]
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Stroke is a major cause of death and disability, with its complex pathological mechanisms posing challenges to effective therapy. Autophagy plays a critical role in cellular homeostasis and survival, with both protective and harmful effects on neuronal cells during ischemic injury. Naturally derived compounds have been found to modulate autophagy and provide neuroprotection against stroke, suggesting potential applications in treatment strategies.
Stroke is considered a leading cause of mortality and neurological disability, which puts a huge burden on individuals and the community. To date, effective therapy for stroke has been limited by its complex pathological mechanisms. Autophagy refers to an intracellular degrading process with the involvement of lysosomes. Autophagy plays a critical role in maintaining the homeostasis and survival of cells by eliminating damaged or non-essential cellular constituents. Increasing evidence support that autophagy protects neuronal cells from ischemic injury. However, under certain circumstances, autophagy activation induces cell death and aggravates ischemic brain injury. Diverse naturally derived compounds have been found to modulate autophagy and exert neuroprotection against stroke. In the present work, we have reviewed recent advances in naturally derived compounds that regulate autophagy and discussed their potential application in stroke treatment. (C) 2021 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
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