{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T11:14:10Z","timestamp":1788088450043,"version":"build-2803163510"},"reference-count":89,"publisher":"Institute of Cytology and Genetics, SB RAS","issue":"5","license":[{"start":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T00:00:00Z","timestamp":1787702400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/vavilov.elpub.ru\/jour\/about\/editorialPolicies#openAccessPolicy"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vestn. VOGiS"],"abstract":"<jats:p>\n                    Cellular senescence is characterized by irreversible cell-cycle arrest, with cells remaining viable and metabolically active. This state features a proinflammatory senescence-associated secretory phenotype (SASP) that can harm neighboring tissues. Accumulation of senescent cells accelerates age-related physiological decline and associated pathologies. Furthermore, cellular senescence is implicated in various physiological processes, including embryonic development, wound healing, tumor progression, and immune response regulation. The complexity of the aging process arises from its diverse underlying mechanisms, potential reversibility, and intrinsic heterogeneity. Experimental gerontology focuses on identifying pathogenic modulators that regulate the formation and accumulation of senescent cells, as well as investigating their impact on tissue function. Within the field of experimental gerontology, considerable attention is devoted to identifying pathogenic modulators that regulate the formation and accumulation of senescent cells, as well as to investigating their impact on tissue function. Of particular interest is the characterization of novel molecular mechanisms that govern cellular aging. Key pathogenic molecular pathways include the p53-dependent senescence pathway, the p16INK4a\/pRb pathway, and non-canonical pathways like IFIH1-MAVS, which contribute to oxidative stress, DNA damage, activation of SASP, and other cellular dysfunction. This study critically examines how viral and bacterial agents induce cellular senescence, particularly\n                    <jats:italic>in vitro<\/jats:italic>\n                    , reviewing the regulatory mechanisms involved. It discusses genetic variants affecting infection susceptibility and categorizes senescence markers. Investigating the molecular mechanisms underlying cellular aging presents promising avenues for the development of targeted and effective therapeutic interventions. Such strategies may include the selective induction of senescence in cancer cells, suppression of senescence to mitigate age-related diseases, or the comprehensive modulation of aging processes to optimize clinical outcomes.\n                  <\/jats:p>","DOI":"10.18699\/vjgb-26-72","type":"journal-article","created":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T09:03:05Z","timestamp":1788080585000},"page":"713-724","source":"Crossref","is-referenced-by-count":0,"title":["Pathogenic modulators of cellular senescence"],"prefix":"10.18699","volume":"30","author":[{"given":"E. V.","family":"Simoroz","sequence":"first","affiliation":[{"name":"Sirius University of Science and Technology, Sirius Federal Territory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y. V.","family":"Antonov","sequence":"additional","affiliation":[{"name":"Sirius University of Science and Technology, Sirius Federal Territory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. S.","family":"Muravyov","sequence":"additional","affiliation":[{"name":"Sirius University of Science and Technology, Sirius Federal Territory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Vasilevska","sequence":"additional","affiliation":[{"name":"Sirius University of Science and Technology, Sirius Federal Territory"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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