Asian Journal of Research in Pharmaceutical Sciences
  • Year: 2023
  • Volume: 13
  • Issue: 1

The Science of Aging and Longevity

  • Author:
  • Sara Sunil Mohite1, Shahbaz Akhtar Momin1, Samip Anant Niwate1, Riya Madanlal Paliwal1,*, Khushboo Chhotelal Yadav1, Shikha Shukla2, Dileep Kumar Bharati3
  • Total Page Count: 7
  • Published Online: Oct 9, 2023
  • Page Number: 33 to 39

1Students, Ideal Institute of Pharmacy, Wada, Palghar, Maharashtra

2Students, Ideal Institute of Pharmacy, Wada, Palghar, Maharashtra

3The Principal, Ideal Institute of Pharmacy, Wada, Palghar, Maharashtra

*Corresponding Author E-mail: riyapaliwal423@gmail.com

Online Published on 09 October, 2023.

Abstract

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contribution to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging with minimal side-effects.

Keywords

Aging, Genetic pathways, Biochemical processes, Hallmarks, Genomic instability, Telomere attrition, Epigenetic alterations, Loss of proteostasis, Deregulated nutrient-sensing, Mitochondrial dysfunction, Cellular senescence, Stem cell exhaustion, Altered intercellular communication