We are analyzing https://link.springer.com/article/10.1007/s12031-025-02313-y.

Title:
Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis | Journal of Molecular Neuroscience
Description:
Ischemic stroke is a leading cause of disability and death worldwide, largely due to its increasing incidence associated with an aging population. This condition results from arterial obstruction, significantly affecting patients
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Keywords {🔍}

pubmed, article, google, scholar, cas, cell, central, death, httpsdoiorgs, zhang, wang, stroke, necroptosis, liu, ischemic, chen, mechanisms, dis, ferroptosis, mitochondrial, mol, zhao, injury, ripk, biol, apoptosis, therapeutic, sci, yang, disease, tang, molecular, activation, huang, pathways, zhou, int, med, sun, xie, role, cerebral, res, lin, target, promotes, signaling, nat, diseases, signal,

Topics {✒️}

pink1/parkin-induced mitochondrial ubiquitination month download article/chapter amp-activated protein kinase cerebral ischemia-reperfusion injury cerebral ischemia/reperfusion injury rip1-rip3-mlkl pathway bcl-2-family protein tbid cerebral ischemia-reperfusion mice hsp90-gcn2-atf4 pathway trimerization-deficient mutant identifies relevant small-molecule compounds trif-mediated cell death bnip3l/nix-mediated mitophagy metal-dependent cell death cardiac ischemia/reperfusion injury calpain-mediated mitochondrial damage p53-mediated ferroptotic responses targeting caspase-8/c-flip full article pdf hepcidin-ferroportin axis tumor suppressor p53 heat shock factor-1 ischemia-reperfusion injury cell death pathways—necroptosis death domain kinase receptor-interacting protein blocking dpp4 activity ampk-mediated phosphorylation regulated cell death ampk-dependent phosphorylation privacy choices/manage cookies systemic iron levels programmed cell death asc oligomerization inhibitor tak1-tabs complex apoptotic death induced related subjects hsp90 inhibition protects tnf-induced necroptosis mol cell biochem ischemic brain injury epicatechin-mediated modulation rhim-mediated interactions zhihao wang wrote ferroptotic cell death neuronal cell death blood flow ampk-parkin-mitophagy tak1-dependent manner central neuropathies

Questions {❓}

Kinnally KW, Peixoto PM, Ryu SY, Dejean LM (2011) Is mPTP the gatekeeper for necrosis, apoptosis, or both?

Schema {🗺️}

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         description:Ischemic stroke is a leading cause of disability and death worldwide, largely due to its increasing incidence associated with an aging population. This condition results from arterial obstruction, significantly affecting patients' quality of life and imposing a substantial economic burden on healthcare systems. While current treatments primarily focus on the rapid restoration of blood flow through thrombolytic therapy or surgical interventions, a limited understanding of neuronal injury mechanisms hampers the development of more effective treatments.This article explores the interplay among various cell death pathways—necroptosis, apoptosis, autophagy, ferroptosis, and pyroptosis—in the context of ischemic stroke to identify novel therapeutic targets. Each mode of cell death displays unique characteristics and roles post-stroke, and the activation of these pathways may vary across different animal models, complicating the translation of therapeutic strategies to clinical settings. Notably, the interaction between apoptosis and necroptosis is highlighted; inhibiting apoptosis might heighten the risk of necroptosis. Therefore, a balanced regulation of these pathways could promote enhanced neuronal survival.Additionally, we introduce PANoptosis, a form of cell death that encompasses pyroptosis, apoptosis, and necroptosis, emphasizing the complexity and potential therapeutic implications of these interactions. In summary, understanding the relationships among these cell death mechanisms in ischemic stroke is vital for developing new neuroprotective agents. Future research should aim for combinatorial interventions targeting multiple pathways to optimize treatment strategies and improve patient outcomes.
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      headline:Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis
      description:Ischemic stroke is a leading cause of disability and death worldwide, largely due to its increasing incidence associated with an aging population. This condition results from arterial obstruction, significantly affecting patients' quality of life and imposing a substantial economic burden on healthcare systems. While current treatments primarily focus on the rapid restoration of blood flow through thrombolytic therapy or surgical interventions, a limited understanding of neuronal injury mechanisms hampers the development of more effective treatments.This article explores the interplay among various cell death pathways—necroptosis, apoptosis, autophagy, ferroptosis, and pyroptosis—in the context of ischemic stroke to identify novel therapeutic targets. Each mode of cell death displays unique characteristics and roles post-stroke, and the activation of these pathways may vary across different animal models, complicating the translation of therapeutic strategies to clinical settings. Notably, the interaction between apoptosis and necroptosis is highlighted; inhibiting apoptosis might heighten the risk of necroptosis. Therefore, a balanced regulation of these pathways could promote enhanced neuronal survival.Additionally, we introduce PANoptosis, a form of cell death that encompasses pyroptosis, apoptosis, and necroptosis, emphasizing the complexity and potential therapeutic implications of these interactions. In summary, understanding the relationships among these cell death mechanisms in ischemic stroke is vital for developing new neuroprotective agents. Future research should aim for combinatorial interventions targeting multiple pathways to optimize treatment strategies and improve patient outcomes.
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