Review: bacterial infections as proposed drivers of cellular senescence and immunosenescence
This review abstract proposes that bacterial pathogens can drive cellular senescence and immunosenescence through genotoxic effects, oxidative stress and disrupted host signaling, linking infections to premature aging; it is a proposed perspective, not a tested intervention. [1]
Automatic summary · not editorially reviewed
The key findings
The review aims to examine changes in senescent cells and critically assess bacterial infections as drivers of immunosenescence. [1]
The abstract names genotoxic effects, oxidative stress and disrupted host signaling as mechanisms by which bacterial pathogens induce senescence. [1]
The work is presented as offering a perspective on infections and premature aging and highlighting potential therapeutic targets. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- Senescent cells, host tissues and immune function in the context of bacterial infection, as discussed in a review
- Summary based on
- Study abstract
- Original publication
- July 22, 2026
Review aim: senescence, aging and bacterial infection
The abstract describes a review that aims to examine cellular and molecular changes in senescent cells and to critically assess the role of bacterial infections as drivers of immunosenescence. It states that the relationship between cellular senescence, aging and host-pathogen interactions remains incompletely understood. The authors present their novelty as integrating current knowledge into direct and indirect mechanisms by which bacterial pathogens induce senescence.
Supporting source [1]
Proposed mechanisms: genotoxic stress and signaling pathways
According to the abstract, the review highlights molecular mechanisms of pathogen-induced stress responses and their impact on host tissues and immune function. It names genotoxic effects, oxidative stress and disruption of host signaling pathways as mechanisms. Particular emphasis is placed on how bacterial virulence factors modulate pathways such as p53-p21, p16-Rb, NF-κB, mTOR and cGAS-STING, thereby promoting a pro-inflammatory senescence-associated secretory phenotype (SASP) and facilitating chronic infection and tissue damage.
Supporting source [1]
Proposed perspective on infections and age-related disease
The abstract says the work links microbial activity with cellular aging processes and offers a novel perspective on how infections may contribute to premature aging and age-related diseases. It also highlights potential therapeutic targets for modulating senescence and improving host resilience. These are proposed perspectives and targets from a review, not demonstrated treatments or measured effects in people.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The abstract reports no study design, sample, follow-up or measured outcomes, and the mechanisms and therapeutic targets are proposed, not demonstrated.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Iordache F, Zaharie AA, Rosu PM, Holban AM, Curutiu C. · europepmc.org · July 22, 2026