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Transcriptional Regulation of Lifespan, Ageing and Age-Related Pathologies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 2566

Special Issue Editor


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Guest Editor
Laboratory of Genome Variation, National Research Centre “Kurchatov Institute”, 123182 Moscow, Russia
Interests: age-related diseases; aging; glycogen synthase kinase; gene expression; transcription factors

Special Issue Information

Dear Colleagues,

It has recently become apparent that the eukaryotic transcriptome is much more complex than the genome, and it is the finely adjustable gene transcription that determines the diversity, intricacy, and specificity of genetic control of all biological processes in the cell and organism. Transcriptome complexity is determined by cellular and tissue-specific transcriptional levels and sets of gene transcripts.

Complex phenotypes are also primarily controlled via the regulation of the transcriptome. For example, it has long been demonstrated that a special program of gene expression controls the progression of successive stages of development. The influence of gene expression on the aging process is thought to be equally important. It has also recently become apparent that naturally occurring genetic variants associated with various human diseases, including age-related diseases, map onto non-coding parts of the genome and are enriched in regulatory gene regions, suggesting that many causative variants may influence gene expression.

The aim of this Special Issue is to bring together original scientific and review articles that present new data, approaches, and perspectives on the role of transcription regulation, alternative cell-specific and age-specific transcripts, and transcriptional networks in controlling lifespan, aging, and senile diseases.

Suggested topics include but are not limited to:

  • Gene expression control as the backbone of lifespan regulation;
  • Gene expression profiles associated with aging and age-related pathologies;
  • Altering transcription factor binding sites as the basis for variation in lifespan, aging rates, and progression of age-related pathologies;
  • Cell-type-specific gene expression levels and patterns in the control of lifespan, aging, and age-related pathologies;
  • The role of alternative gene transcripts in controlling lifespan;
  • Transcriptional networks regulating lifespan, aging, and age-related pathologies.

Dr. Elena Genrikhovna Pasyukova
Guest Editor

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Keywords

  • gene regulation
  • gene expression
  • transcription factors binding sites
  • differential transcription
  • alternative gene transcripts
  • transcription networks
  • lifespan and aging
  • age-related pathologies
  • complex traits

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Published Papers (1 paper)

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Research

11 pages, 1482 KiB  
Communication
P38 MAPK Signaling in the Retina: Effects of Aging and Age-Related Macular Degeneration
by Natalia A. Muraleva and Nataliya G. Kolosova
Int. J. Mol. Sci. 2023, 24(14), 11586; https://doi.org/10.3390/ijms241411586 - 18 Jul 2023
Cited by 7 | Viewed by 2256
Abstract
Age-related macular degeneration (AMD) is the leading cause of irreversible visual impairment worldwide. Age is the greatest risk factor for AMD but the underlying mechanism remains unascertained, resulting in a lack of effective therapies. Growing evidence shows that dysregulation of the p38 MAPK [...] Read more.
Age-related macular degeneration (AMD) is the leading cause of irreversible visual impairment worldwide. Age is the greatest risk factor for AMD but the underlying mechanism remains unascertained, resulting in a lack of effective therapies. Growing evidence shows that dysregulation of the p38 MAPK signaling pathway (SP) contributes to aging and neurodegenerative diseases; however, information about its alteration in the retina with age and during AMD development is limited. To assess the contribution of alterations in p38 MAPK signaling to AMD, we compared age-associated changes in p38 MAPK SP activity in the retina between Wistar rats (control) and OXYS rats, which develop AMD-like retinopathy spontaneously. We analyzed changes in the mRNA levels of genes of this SP in the retina (data of RNA-seq) and evaluated the phosphorylation/activation of key kinases using Western blotting at different stages of AMD-like pathology including the preclinical stage. p38 MAPK SP activity increased in the retinas of healthy Wistar rats with age. The manifestation and dramatic progression of AMD-like pathology in OXYS rats was accompanied by hyperphosphorylation of p38 MAPK and MK2 as key p38 MAPK SP kinases. Retinopathy progression co-occurred with the enhancement of p38 MAPK-dependent phosphorylation of CryaB at Ser59 in the retina. Full article
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