Advances in Ageing: From Molecular Mechanism to Strategies
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 12008
Special Issue Editor
Special Issue Information
Dear Colleagues,
The process of ageing is related to molecular damage slowly accumulating with age since the mechanisms responsible for the repair or removal of the damage become more and more ineffective with advancing age. DNA damage occurs as a result of replication errors, intrinsic stress associated with reactive oxygen species (ROS) and extrinsic stress (e.g., UV light and irradiation). The DNA damage response (DDR) signalling pathway coordinated by the ATM and ATR kinases involved in the repair of the majority of DNA damage; however, the accumulation of unrepaired damages may lead to apoptosis, and cellular senescence or cancer.
Various hallmarks of ageing have been identified so far, including telomeres shortening, dysregulated mitochondrial metabolism, epigenetic modifications, proteostasis, inflammageing, cell-matrix interactions, stem cell exhaustion, dysregulated nutrient sensing and immuno-senescence. Both increased ROS levels and dysfunctional mitochondria have been found to be associated with age and age-related diseases. Protein homoeostasis as well as the proper functioning of quality control systems involved in protein synthesis, folding and refolding are crucial for cellular function. The decreasing (with age) efficiency of the autophagic and proteasomal systems for protein degradations results in the accumulation of damaged protein probably fuelling a self-amplifying cycle of impairment. The results of studies provided evidence for the involvement of damaged proteins in the process of ageing. The exhaustion or loss of function of stem cells and impaired intercellular communication contribute to age-related deterioration of tissue regeneration abilities.
Our understanding of the molecular mechanisms underlying aging is constantly improving; however, still there are gaps that require additional research. The utilization of microarrays and sequencing techniques provides new information that improves our understanding of genome as well as cellular, tissue, and organ-specific transcriptomes. Growing evidence shows that long noncoding RNAs (lncRNAs) are involved in cellular senescence at transcriptional, post-transcriptional, translational, and post-translational levels. Our lifespan has improved, but our health span (defined as years of healthy living) still falls due to age-related diseases, including cardiovascular disease (CVD), chronic kidney disease (CKD), neurodegenerative disorders, cancers, type 2 diabetes, obesity, etc.
Understanding the underlying physiology of aging is essential for delaying both aging and the onset of multiple age-related diseases. This Special Issue focuses on novel mechanisms involved in aging and possible strategies to delay this process.
Dr. Anna Gluba-Sagr
Guest Editor
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Keywords
- ageing
- telomeres shortening
- dysregulated mitochondrial metabolism
- epigenetic modifications
- proteostasis
- inflammageing
- cell-matrix interactions
- stem cell exhaustion
- dysregulated nutrient sensing
- immuno-senescence
- age-related diseases
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