Modulating autophagy and mitophagy as a promising therapeutic approach in neurodegenerative disorders.

Gurjit Kaur Bhatti, Jasvinder Singh Bhatti, Arubala P Reddy, Arti Singh, Jayapriya Mishra, Abhishek Sehrawat, Charan Singh, P Hemachandra Reddy

Journal: Life sciences 2022;311(Pt A):121153

PMID: 36343743

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Abstract

The high prevalence of neurodegenerative diseases has become a major public health challenge and is associated with a tremendous burden on individuals, society and federal governments worldwide. Protein misfolding and aggregation are the major pathological hallmarks of several neurodegenerative disorders. The cells have evolved several regulatory mechanisms to deal with aberrant protein folding, namely the classical ubiquitin pathway, where ubiquitination of protein aggregates marks their degradation via lysosome and the novel autophagy or mitophagy pathways. Autophagy is a catabolic process in eukaryotic cells that allows the lysosome to recycle the cell's own contents, such as organelles and proteins, known as autophagic cargo. Their most significant role is to keep cells alive in distressed situations. Mitophagy is also crucial for reducing abnormal protein aggregation and increasing organelle clearance and partly accounts for maintaining cellular homeostasis. Furthermore, substantial data indicate that any disruption in these homeostatic mechanisms leads to the emergence of several age-associated metabolic and neurodegenerative diseases. So, targeting autophagy and mitophagy might be a potential therapeutic strategy for a variety of health conditions.

Address: Laboratory of Translational Medicine and Nanotherapeutics, Department of Human Genetics and Molecular Medicine, School of Health Sciences, Central University of Punjab, Bathinda, India.; Department of Medical Lab Technology, University Institute of Applied Health Sciences, Chandigarh University, Mohali, India.; Department of Pharmaceutics, ISF College of Pharmacy, Moga, Punjab, India.; Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.; Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Pharmacology and Neuroscience and Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.; Laboratory of Translational Medicine and Nanotherapeutics, Department of Human Genetics and Molecular Medicine, School of Health Sciences, Central University of Punjab, Bathinda, India. Electronic address: [email protected].

DOI: 10.1016/j.lfs.2022.121153

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MeSH Terms: Humans, Mitophagy, Autophagy, Neurodegenerative Diseases, Lysosomes, Ubiquitin