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Journal of Advanced Research xxx (xxxx) xxxContents lists available at ScienceDirect Journal of Advanc ed Research journal homepag e: www.elsevier .com/locate / jare Intracellular mitochondrial transfer in ischemic stroke: Mechanisms and therapeutic applicationAbbreviations: ARF1, ADP-ribosylation factor 1; BBB, blood–brain barrier; BDNF, brain-derived neurotrophic factor; BECs, brain endothelial cells; BMSCs, bone derived mesenchymal stem cells; cADPR, cyclic ADP ribose; CBF, cerebral blood flow; cGAS, cyclic GMP-AMP Synthase; CNS, central nervous system; Cx32, connexin 3 connexin 43; Dmp1, dentin matrix protein 1; Drp1, dynamically-associated protein 1; cAMP, cyclic adenosine monophosphate; ECs, endothelial cells; EPCs, en progenitor cells; ER, endoplasmic reticulum; EVs, extracellular vesicles; Fis1, mitochondrial fission 1 protein; GJCs, gap junction channels; GSH, glutathione; hNSCs neural stem cells; IL-1b, interleukin-1beta; IMM, inner Mitochondrial Membrane; IS, ischemic stroke; LRP1, low-density lipoprotein receptor-related protein mitochondrial biogenesis; Mfn1, mitofusins 1; Mfn2, mitofusins 2; Miro1, mitochondrial Rho GTPase 1; MMP, mitochondrial membrane potential; MMSCs, mu mesenchymal stem cells; mPTP, mitochondrial permeability transition pore; MSCs, mesenchymal stem cells; mtDNA, mitochondrial DNA; mtROS, mitochondrial oxygen species; OGD, oxygen-glucose deprivation; OGD/R, OGD-reperfusion; OLs, oligodendrocyte; OMM, outer mitochondrial membrane; OPA1, optic atrophy oligodendrocyte precursor cells; ox-mtDNA, oxidative mtDNA; PGC-1a, peroxisome proliferator-activated receptor coactivator a; PINK1, PTEN induced kinase 1; permanent middle cerebral artery occlusion; STING, stimulator of interferon genes; TCA, tricarboxylic acid; tMCAO, transient middle cerebral artery occlusion; TNF- necrosis factor-alpha; TNTs, tunneling nanotubes; Trkb, tyrosine kinase beta; UC-MSCs, umbilical cord MSCs. ⁎ Corresponding authors. E-mail addresses: zhoums1963@163.com (M.-s. Zhou), yueyangliu1989@163.com (Y. Liu). https://doi.org/10.1016/j.jare.2026.03.037 2090-1232/© 2026 The Author(s). Published by Elsevier B.V. on behalf of Cairo University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article as: R. Fu, Y. Zhao, Y. Li et al., Intracellular mitochondrial transfer in ischemic stroke: Mechanisms and therapeutic application, of Advanced Research, https://doi.org/10.1016/j.jare.2026.03.037Rong Fu a , a Science and Experiment Research Center & Shenyang Key Laboratory of Vascular Biology, Shenyang Medical College, Shenyang, China Yang Zhao b , b Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, China Yayi Li a , Yuliang Zhang a , Meidan Wang c , c Department of Vasculocardiology, The Second Hospital of Shenyang Medical College, Shenyang, China Zhuo Wang a,d , d General Hospital of Northern Theater Command, Shenyang, China Ming-sheng Zhou a,⁎ , Yueyang Liu e,⁎ e Department of Pharmacology, Shenyang Medical College, Shenyang, Chinah i g h l i g h t s • Summary of latest researches on IS- induced mitochondrial dysfunction. • Overview of the healthy and damaged mitochondrial transfer among endogenous neural cells following IS. • Overview of the healthy mitochondria donated by stem cell to treat IS. • Discussion of the current issues and challenges pertaining to mitochondrial transfer.g r a p h i c a l a b s t r a c ta r t i c l e i n f o Article history: Received 4 January 2025 Revised 11 March 2026 Accepted 15 March 2026 Available online xxxx Keywords: Cell to cell communication Ischemic stroke a b s t r a c t Background: Current therapeutic models for ischemic stroke (IS) are shifting from a narrow focus on neu- roprotection to a broader concept of cytoprotection. This new paradigm emphasizes rescuing damaged brain cells and maintaining their structural and functional integrity t