The aging process results from accumulation of molecular damage and impairment of signalling pathways that affect not only single cells but also organs and whole individuals. Besides physiological modifications along time, the aging phenotype can be accelerated by metabolic dysfunction. Aging and metabolic dysfunction phenotypes share biomarkers as well as initial and progression mechanisms.

We invite authors to submit original research and review articles (in vitro, animal, and/or clinical studies) for publishing in this special issue, focused not only on individual hallmarks of senescent cells, responses to age-related damage, aging phenotype, and age-associated diseases but also on their sequential evolution and interconnection. Studies on metabolic dysfunction contribution to the earlier development of aging features as well as counteracting strategies could also be considered for submission.

Potential topics include, but are not limited to:

• Cellular biomarkers of aging:
  • Gene expression and epigenetic regulation
  • Posttranslational modification and proteostasis loss
  • Mitochondrial dysfunction and disruption of redox signalling
  • Cellular senescence, genomic instability, and telomere attrition
• Organ and peripheral biomarkers of aging:
  • The immune system and aging (autoimmune responses, immunological memory, and chronic low-grade inflammation)
  • Early developmental (epigenetic) programming of aging and modulation by the environment
  • Premature aging associated with insulin resistance
  • Aging and cardiovascular, neurodegenerative, and cognitive impairment disease risk
• Antiaging strategies:
  • Antiaging nutrients and energy restriction mimetics