Journal of visualized experiments : JoVEOct 31, 2026

Cell Death Processes in Stroke: From How They Work to Possible Treatments

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Nov 2, 2026

Abstract

Ischemic stroke involves multiple interconnected processes that may contribute to cellular injury.

Bioenergetic failure, excitotoxicity, and ionic imbalances are observed in the ischemic core and penumbra.
Cell death mechanisms like apoptosis, necroptosis, and ferroptosis are associated with experimental ischemic injury.
Autophagy plays a critical role in maintaining cellular health and may influence various cell death pathways.
Pathway interactions and shared molecular targets are identified, including mitochondrial function and inflammatory signaling.
Preclinical interventions are evaluated based on their specific models and outcomes, but clinical efficacy and safety remain unproven.

Simplified

Ischemic stroke involves a complex network of interconnected processes, including bioenergetic failure, excitotoxicity, ionic dyshomeostasis involving Na+, K+, Ca2+, and Cl-, oxidative stress, DNA damage, and neurovascular dysfunction. Apoptosis, necroptosis, pyroptosis, ferroptosis, and parthanatos contribute to experimental ischemic injury with different levels of mechanistic support. Autophagy primarily maintains cellular homeostasis and modulates these pathways. Autophagy-dependent cell death requires separate evidence that the autophagic machinery causes death. These processes operate across the ischemic core and penumbra and evolve during ischemia, reperfusion, and recovery. Their effects extend beyond neurons to microglia, astrocytes, brain microvascular endothelial cells, pericytes, and other neurovascular components. This narrative review evaluates pathway execution, shared molecular nodes, and the spatial and temporal limits of the available evidence. It emphasizes receptor-complex regulation, mitochondrial and lysosomal function, phospholipid peroxidation, DNA damage, and inflammatory signaling as points of convergence. Preclinical interventions are assessed according to their models, molecular endpoints, and functional outcomes. A cell- and stage-specific network perspective supports the development of targeted therapies, while the efficacy and safety of coordinated pathway intervention in patients remain to be established.

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Cell Death Processes in Stroke: From How They Work to Possible Treatments

Abstract

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