EC Neurology

Review Article Volume 16 Issue 10 - 2024

Stroke Pathogenesis: Unravelling the Complex Interplay of Autophagy, Oxidative Stress, and Inflammation

Onyinoyi Bethel Onimisi1, Moses Ibrahim Auza2, Joy Ochai3, Stephen Samuel Lazarus4, James Bolaji Promise5, Helena Fodeke6, Muhammad Shehu Hassan6 and Wusa Makena7

1Department of Anatomy, Faculty of Basic Medical Science, Usmanu Danfodiyo University, Sokoto, Nigeria
2Department of Anatomy, Faculty of Basic Medical Science, College of Medicine and Allied Health Sciences, Bingham University Karu, Nasarawa State, Nigeria
3Department of Anatomy, College of Basic Medical Sciences, Federal University of Health Sciences, Otukpo, Benue State, Nigeria
4Department of Basic Medical Science, Faculty of Basic Medical and Health Sciences, New Gate University, Minna, Nigeria
5Department of Nursing Science, College of Health, Joseph Ayo Babalola University, Nigeria
6Department of Public Health, Ahmadu Bello University, Zaria, Nigeria
7Department of Anatomy, Faculty of Basic Medical Science, Kampala International University, Western Campus, Bushenyi, Uganda

*Corresponding Author: Moses I Auza, Department of Human Anatomy, Faculty of Basic Medical Sciences, Bingham University Karu, Nigeria.
Received: August 22, 2024; Published: September 25, 2024



Stroke has caused far more deaths and disabilities than any other health problem, necessitating a comprehensive understanding of its pathophysiology that is crucial to developing effective therapeutic strategies. This review paper examines the complex relationship between stroke, autophagy, oxidative stress and inflammation highlighting their involvement in neuronal injury and therapy. The role that autophagy plays in stroke can be seen in different lights as it can either protect cells by removing damaged organelles or cause cell death when certain conditions prevail. Stroke pathogenesis is determined by major pathways, such as mTOR, NF-κB, and HIF-1, as well as their relationship to ischemic and pro-inflammatory responses. Oxidative stress in stoke, primarily caused by an imbalance in reactive oxygen species (ROS), is a major factor in neuronal damage caused by mitochondrial dysfunction and lipid peroxidation. The significance of antioxidant therapy is an increase in stroke management with oxidative stress as the mediator of cell death. Activation of microglial cells and release of cytokines resulting in inflammatory upsurge increase tissue damage after stroke. Inflammatory response combined with overactive autophagy/oxidative stress may heighten the severity of cerebrovascular disease; thus, neuroprotection can be significantly achieved through maintaining brain antioxidant and anti-inflammatory activities while responding to injury. Obstacles including translation gaps and individual variations in treatment response necessitate more research to clarify the signaling pathways' roles and identify new therapeutic targets.

Keywords: Ischemia; Stroke; Autophagy; Inflammation; Oxidative Stress; Neurodegeneration

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Onyinoyi Bethel Onimisi., et al. “Stroke Pathogenesis: Unravelling the Complex Interplay of Autophagy, Oxidative Stress, and Inflammation”. EC Neurology  16.10 (2024): 01-19.