Role of the AMPK signalling pathway in the aetiopathogenesis of ocular diseases
Document Type
Article
Publication Title
Human and Experimental Toxicology
Abstract
Background: AMP-activated protein kinase (AMPK) plays a precise role as a master regulator of cellular energy homeostasis. AMPK is activated in response to the signalling cues that exhaust cellular ATP levels such as hypoxia, ischaemia, glucose depletion and heat shock. As a central regulator of both lipid and glucose metabolism, AMPK is considered to be a potential therapeutic target for the treatment of various diseases, including eye disorders. Objective: To review all the shreds of evidence concerning the role of the AMPK signalling pathway in the pathogenesis of ocular diseases. Method: Scientific data search and review of available information evaluating the influence of AMPK signalling on ocular diseases. Results: Review highlights the significance of AMPK signalling in the aetiopathogenesis of ocular diseases, including cataract, glaucoma, diabetic retinopathy, retinoblastoma, age-related macular degeneration, corneal diseases, etc. The review also provides the information on the AMPK-associated pathways with reference to ocular disease, which includes mitochondrial biogenesis, autophagy and regulation of inflammatory response. Conclusion: The study concludes the role of AMPK in ocular diseases. There is growing interest in the therapeutic utilization of the AMPK pathway for ocular disease treatment. Furthermore, inhibition of AMPK signalling might represent more pertinent strategy than AMPK activation for ocular disease treatment. Such information will guide the development of more effective AMPK modulators for ocular diseases. (Figure presented.).
DOI
10.1177/09603271211063165
Publication Date
1-7-2022
Recommended Citation
Shukal, Dhaval K.; Malaviya, Pooja B.; and Sharma, Tusha, "Role of the AMPK signalling pathway in the aetiopathogenesis of ocular diseases" (2022). Open Access archive. 4692.
https://impressions.manipal.edu/open-access-archive/4692