Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 26 min ago
Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Mitochondrial cristae remodeling in ischemic stroke: mechanisms and therapeutic perspectives

  • Dawei Zhang1,2
  • Hongbo Zhang1
  • Ruoxin Tu1
  • Shuo Zhang1
  • Hao Tian1
  • Yue Meng2
  • Xiaolin Lv2
  • Hongna Yin2
  1. 1Heilongjiang University of Chinese Medicine
  2. 2The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine
Open at sourcePDFDOICite

Abstract

Mitochondrial cristae arrange the respiratory machinery within the inner membrane and change as ischemia gives way to reperfusion. Their organization depends on mitochondrial contact site and cristae organizing system assemblies, optic atrophy 1, adenosine triphosphate synthase, and cardiolipin. Disruption of these systems can impair energy production, facilitate neuronal death, and expose mitochondrial DNA to inflammatory sensors. This review brings structural work together with experimental stroke studies to examine how crista remodeling contributes to injury and recovery. Genetic manipulation of selected regulators has preserved mitochondrial structure and reduced injury in neurons and microglia. Most of these interventions preceded ischemia, leaving the speed and feasibility of repair after stroke onset uncertain. Pharmacological modulation and mitochondrial delivery offer ways to address this gap, particularly around reperfusion. Emerging strategies combine modulation of crista protein assemblies with cardiolipin directed treatment, mitochondrial antioxidant nanomedicine, organelle delivery, and control of local drug exposure. Their therapeutic evaluation can be aligned with distinct opportunities at reperfusion and during subsequent tissue recovery. Progress toward treatment will require evidence that a candidate reaches the affected brain cells, modifies the intended membrane assembly, and produces lasting neurological benefit. The available studies place crista remodeling within neuroprotective pathways and identify the experimental steps needed to evaluate it as a therapeutic target.

Related

  1. Metabolic Remodeling in Peritoneal Dialysis-Associated Peritoneal Fibrosis: Mechanisms, Candidate Metabolic Signatures, and Therapeutic Perspectives
    Zhengjie Zhu, Mengyang Wang, Tao Zhang +3
    MetabolitesPeer-reviewedCC BYFull textProteomics & metabolomicsEurope PMC
  2. Bidirectional mitochondrial transfer in the osteoimmune microenvironment: mechanisms and therapeutic perspectives
    Lei Huang, Xin Chen, Yuqin Guo +5
    Frontiers in EndocrinologyPeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationCrossrefEurope PMCPMCEurope PMC
  3. AAV9 Gene Therapy for Ovarian Dysfunction and Reproductive Aging: Molecular Mechanisms, Therapeutic Targets, and Translational Perspectives
    Safeer Ullah, Imran Ullah, Beshoy Sameh Fawzy Khalil +8
    International journal of molecular sciencesPeer-reviewedCC BYFull textGeneral biochemistryEurope PMC
  4. Mitochondrial Dynamics in Diabetes Mellitus and Its Complications: Mechanisms, Pathological Roles, and Therapeutic Implications.
    Guohua Wang, Yige Zhao, Gaiting Liu +5
    International journal of molecular sciencesPeer-reviewedCC BYFull textMolecular biology & gene regulationEurope PMC
  5. Microbial metabolite-mediated gut–liver axis remodeling after hepatectomy: mechanisms and therapeutic opportunities
    Chao Ji, Jing Zhang, Yan Jiao
    Frontiers in surgeryPeer-reviewedCC BYFull textMolecular biology & gene regulationEurope PMCPMCEurope PMC

Cite

BibTeXRIS
BibTeX
@article{zhang2026mitochondrial,
  title = {{Mitochondrial cristae remodeling in ischemic stroke: mechanisms and therapeutic perspectives}},
  author = {Dawei Zhang and Hongbo Zhang and Ruoxin Tu and Shuo Zhang and Hao Tian and Yue Meng and Xiaolin Lv and Hongna Yin},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.2017406},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.2017406/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Mitochondrial cristae remodeling in ischemic stroke: mechanisms and therapeutic perspectives
AU  - Dawei Zhang
AU  - Hongbo Zhang
AU  - Ruoxin Tu
AU  - Shuo Zhang
AU  - Hao Tian
AU  - Yue Meng
AU  - Xiaolin Lv
AU  - Hongna Yin
PY  - 2026
DA  - 2026/10/26
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.2017406
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.2017406/full
AB  - Mitochondrial cristae arrange the respiratory machinery within the inner membrane and change as ischemia gives way to reperfusion. Their organization depends on mitochondrial contact site and cristae organizing system assemblies, optic atrophy 1, adenosine triphosphate synthase, and cardiolipin. Disruption of these systems can impair energy production, facilitate neuronal death, and expose mitochondrial DNA to inflammatory sensors. This review brings structural work together with experimental stroke studies to examine how crista remodeling contributes to injury and recovery. Genetic manipulation of selected regulators has preserved mitochondrial structure and reduced injury in neurons and microglia. Most of these interventions preceded ischemia, leaving the speed and feasibility of repair after stroke onset uncertain. Pharmacological modulation and mitochondrial delivery offer ways to address this gap, particularly around reperfusion. Emerging strategies combine modulation of crista protein assemblies with cardiolipin directed treatment, mitochondrial antioxidant nanomedicine, organelle delivery, and control of local drug exposure. Their therapeutic evaluation can be aligned with distinct opportunities at reperfusion and during subsequent tissue recovery. Progress toward treatment will require evidence that a candidate reaches the affected brain cells, modifies the intended membrane assembly, and produces lasting neurological benefit. The available studies place crista remodeling within neuroprotective pathways and identify the experimental steps needed to evaluate it as a therapeutic target.
SN  - 1663-9812
ER  -