Academic Journal

Cellular senescence in ischemic stroke: Cell-type specificity, temporal dynamics, and response to therapeutic interventions.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Cellular senescence in ischemic stroke: Cell-type specificity, temporal dynamics, and response to therapeutic interventions.
Συγγραφείς: Liu X; Department of Neurology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany., Guo Y; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China., Popa-Wagner A; Center for Normal and Pathological Ageing, University of Medicine and Pharmacy, Craiova, Romania., Lämmermann I; Rockfish Bio AG, Vienna, Austria., Grillari J; Ludwig Boltzmann Institute for Traumatology, the Research Center in Cooperation with AUVA, Vienna, Austria; Institute of Molecular Biotechnology, BOKU University, Vienna, Austria; Austrian Cluster for Tissue Regeneration, Vienna, Austria. Electronic address: johannes.grillari@boku.ac.at., Hermann DM; Department of Neurology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany. Electronic address: dirk.hermann@uk-essen.de.
Πηγή: Ageing research reviews [Ageing Res Rev] 2026 Aug; Vol. 120, pp. 103206. Date of Electronic Publication: 2026 Jun 14.
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Science Country of Publication: England NLM ID: 101128963 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-9649 (Electronic) Linking ISSN: 15681637 NLM ISO Abbreviation: Ageing Res Rev Subsets: MEDLINE
Imprint Name(s): Original Publication: Oxford, UK : Elsevier Science, c2002-
Ιατρικοί όροι (MeSH): Cellular Senescence*/physiology , Ischemic Stroke*/pathology , Ischemic Stroke*/metabolism , Ischemic Stroke*/therapy , Brain*/pathology , Brain*/metabolism , Brain Ischemia*/pathology , Stroke*/pathology, Humans ; Animals ; Senescence-Associated Secretory Phenotype
Περίληψη: Increasing experimental and clinical evidence indicates activation of cellular programs resembling senescence and senescence-associated secretory phenotype signaling after stroke. However, a central challenge is definitional: in injured brain tissue, many senescence-associated features overlap with acute stress responses, transient cell-cycle perturbations, and reactive glial or vascular programs, complicating interpretation across models, time points, and cell types. Here, we synthesize the literature using a cell-type-resolved framework spanning acute, subacute, and chronic stroke phases across major neurovascular and immune compartments. Rather than treating senescence as a binary fate, we conceptualize post-stroke senescence-associated biology as a dynamic continuum, in which ischemia-reperfusion stress engages multiple senescence-related domains, only a subset of which may stabilize into durable cell senescence. Accordingly, we emphasize convergent multi-domain evidence with spatial and cell identity resolution, and cautious use of the term "senescence-like" during early injury. Finally, we discuss translational implications through a timing- and safety-aware perspective, arguing that modulation of maladaptive secretory outputs may be superior to cell-elimination strategies in early post-stroke windows. We highlight key biological and clinical uncertainties-including blood-brain barrier dynamics, hemorrhagic and infectious risk, and interference with endogenous repair-that define critical risk gates for evaluating senescence-targeting approaches after stroke.
(Copyright © 2026 The Authors. Published by Elsevier B.V. All rights reserved.)
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Contributed Indexing: Keywords: Cellular senescence; Ischemic stroke; Neurovascular unit; Senescence-associated secretory phenotype; Temporal dynamics; Therapeutic window
Entry Date(s): Date Created: 20260614 Date Completed: 20260708 Latest Revision: 20260708
Update Code: 20260708
DOI: 10.1016/j.arr.2026.103206
PMID: 42289192
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1872-9649
DOI:10.1016/j.arr.2026.103206