Effect of Ageing and Inflammation on Immune Regulatory Pathway

A Special Issue of Biology (ISSN 2079-7737) belonging to the section "Immunology".

Deadline for manuscript submissions: 31 December 2027 | Viewed by 589

Editors


E-Mail Website
Guest Editor
Futuristic Science Research Center, School of Science, Walailak University, Thasala, Nakhon Si Thammarat 80160, Thailand
Interests: macrophage senescence; mitochondria; SASP; longevity

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Guest Editor
1. Quantitative Biosciences Institute (QBI), University of California San Francisco, San Francisco, CA, USA
2. Gladstone Institute of Data Science and Biotechnology, J. David Gladstone Institutes, San Francisco, CA, USA
3. Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA, USA
Interests: membrane proteins; proteomics; protein-protein interaction; transporters complex; ADP-ribosylome

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Guest Editor Assistant
Akkhraratchakumari Veterinary College, Walailak University, Nakhon Si Thammarat 80160, Thailand
Interests: systems biology; multi-omics; machine learning; cancer

Special Issue Information

Dear Colleagues,

Chronic inflammation plays a pivotal role in aging, with each influencing the other negatively. The inflammatory pathway has been shown to be crucial in determining whether aging is exacerbated. Consequently, the regulatory pathways of inflammation are tightly controlled; any dysregulation may lead to adverse biological outcomes known as inflammaging. Furthermore, cellular senescence represents a significant aspect of aging, where its accumulation profoundly impacts the development of both aging and inflammaging. As we age, our cells are increasingly exposed to environmental cues that contribute to mitochondrial damage. Consequently, accumulated damaged mitochondria can serve as a source of stress molecules, which may amplify inflammaging and ultimately lead to chronic inflammation-related diseases, including cancer. Mitochondrial dysfunction is now recognized as a key hallmark driving cellular senescence.

However, our focus extends beyond mitochondrial dysfunction to include other critical hallmarks, such as nutritional deprivation, telomere shortening, DNA damage responses, and loss of proteostasis. A comprehensive understanding of the inflammatory pathway, as mentioned above, could enable us to monitor how our cells undergo senescence and identify candidate pathways for intervention. Naturally occurring aging in organisms is associated with cellular senescence; thus, maintaining cellular senescence homeostasis could support lifespan and longevity. Our Special Issue encompasses a variety of topics ranging from the molecular basis of cellular senescence, cancer in aging, chronic inflammation, mitochondrial biology in senescence, to longevity. However, our scope is not limited to these key events; we also encourage novel insights on aging, chronic inflammation, and longevity.

Dr. Thiranut Jaroonwitchawan
Dr. Pornparn Kongpracha
Guest Editors

Dr. Tanakamol Mahawan
Guest Editor Assistant

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Keywords

  • aging
  • cellular senescence
  • mitochondria dysfunction
  • inflammation
  • longevity

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Published Papers (1 paper)

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Review

23 pages, 1302 KB  
Review
SIRT1 in Senescence: Mitochondria and Immune Crosstalk
by Jirapat Namkaew, Pornparn Kongpracha, Tanakamol Mahawan and Thiranut Jaroonwitchawan
Biology 2026, 15(18), 1573; https://doi.org/10.3390/biology15181573 - 8 Sep 2026
Viewed by 412
Abstract
Cellular senescence is one of the hallmarks of aging. These growth-arrested cells actively secrete inflammatory mediators that reshape the tissue microenvironment and fuel age-related pathology. Sirtuin 1 (SIRT1) is an NAD+-dependent deacetylase that regulates senescence largely through its control over mitochondrial [...] Read more.
Cellular senescence is one of the hallmarks of aging. These growth-arrested cells actively secrete inflammatory mediators that reshape the tissue microenvironment and fuel age-related pathology. Sirtuin 1 (SIRT1) is an NAD+-dependent deacetylase that regulates senescence largely through its control over mitochondrial integrity and inflammatory signaling. SIRT1 levels and activity fall with age, and this decline directly promotes senescence. SIRT1 maintains mitochondrial function through three interconnected pathways: PGC-1α-driven mitochondria biogenesis, FOXO-dependent antioxidant defense, and mitophagic clearance of damaged organelles. When SIRT1 activity is in an unsteady state, mitochondria become unhealthy. This leads to excessive ROS generation and the leakage of mitochondrial DNA (mtDNA) into the cytosol, which activates the innate immune pathway, consequently resulting in the production of inflammatory cytokines that further inhibit SIRT1. This self-amplifying loop drives cells to irreversible senescence. In this study, we integrate the current understanding of the SIRT1–mitochondria–immune axis within the framework of senescence by examining the biological roles of SIRT1 and the mechanisms that lead to its reduction with aging, while also exploring the interrelated mitochondrial pathways and inflammatory signaling. Furthermore, we assess possible therapeutic strategies targeting this axis and highlight essential questions that necessitate additional research. Full article
(This article belongs to the Special Issue Effect of Ageing and Inflammation on Immune Regulatory Pathway)
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