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Autophagy Coupling Interplay: Can Improve Cellular Repair and Aging?

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Abstract

Regular protein synthesis is a needful and complex task for a healthy cell. Improper folding leads to the deposition of misfolded proteins in cells. Autophagy and ubiquitin–proteasome system (UPS) are the conserved intracellular degradation processes of eukaryotic cells. How exactly these two pathways cross talk to each other is unclear. We do not know how the impairment of autophagy or UPS leads to the disturbance in cellular homeostasis and contribute into cellular aging and neurodegeneration. Here in this review, we will focus on the functional interconnections of autophagy and UPS, and why their loss of function results in abnormal aggregation of misfolded proteotoxic species in cells. Finally, we enumerate and discuss the crucial inducers of autophagy pathways and elaborate their intersection steps, which have been considered to be advantageous in aging linked with the abnormal protein aggregation. The final goal of this review is to improve our current understanding about multifaceted properties and interactions of autophagy and UPS, which may provide new insights to identify novel therapeutic strategies for aging and neurodegenerative diseases.

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Acknowledgments

This work was supported by the Department of Biotechnology, Government of India. AM was supported by Ramalinganswami Fellowship and Innovative Young Biotechnologist Award (IYBA) scheme from the Department of Biotechnology, Government of India. The authors would like to thank Mr. Bharat Pareek and Mr. Rahul Sathya Babu for their technical assistance and the entire lab management during the manuscript preparation. We apologize to various authors whose work could not be included due to space limitations.

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The authors declare no conflicts of interest.

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Chhangani, D., Chinchwadkar, S. & Mishra, A. Autophagy Coupling Interplay: Can Improve Cellular Repair and Aging?. Mol Neurobiol 49, 1270–1281 (2014). https://doi.org/10.1007/s12035-013-8599-z

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