We are analyzing https://link.springer.com/article/10.1007/s10495-021-01661-5.

Title:
New insights into targeting mitochondria in ischemic injury | Apoptosis
Description:
Stroke is the leading cause of adult disability and death worldwide. Mitochondrial dysfunction has been recognized as a marker of neuronal death during ischemic stroke. Maintaining the function of mitochondria is important for improving the survival of neurons and maintaining neuronal function. Damaged mitochondria induce neuronal cell apoptosis by releasing reactive oxygen species (ROS) and pro-apoptotic factors. Mitochondrial fission and fusion processes and mitophagy are of great importance to mitochondrial quality control. This paper reviews the dynamic changes in mitochondria, the roles of mitochondria in different cell types, and related signaling pathways in ischemic stroke. This review describes in detail the role of mitochondria in the process of neuronal injury and protection in cerebral ischemia, and integrates neuroprotective drugs targeting mitochondria in recent years, which may provide a theoretical basis for the progress of treatment of ischemic stroke. The potential of mitochondrial-targeted therapy is also emphasized, which provides valuable insights for clinical research.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, mitochondrial, cell, mitochondria, stroke, wang, brain, ischemic, zhang, injury, biol, cells, chen, ischemia, res, neuronal, httpsdoiorgs, apoptosis, death, neurosci, cerebral, sci, activation, liu, autophagy, role, mol, oxygen, fission, signaling, reactive, yang, pathway, function, neurons, species, mitophagy, potential, damage, drp, neuroprotection, biophys, protein, nature, med,

Topics {✒️}

camp/creb-cd39-dependent manner phospho-ubiquitin-induced parkin activation dl-3-n-butylphthalide induced neuroprotection amp-activated protein kinase mapk-erk-yap signaling pathways month download article/chapter chronic β-ar stimulation weiwei yu & yining huang reactive oxygen species tissue plasminogen activator blood-brain barrier dysfunction disease-related proteins pink1 akt-dependent survivin activation stem cell-induced biobridges akt regulates β-catenin amino-terminal neh2 domain mitochondrial fission-fusion proteins cyclosporine a-induced apoptosis central nervous system calcium-induced mitochondrial dysfunction transforming growth factor-beta cardiomyocyte ischemia/reperfusion-injury pi3k/akt signal pathways cerebral ischemia-reperfusion injury emerging functional cross-talk increased bnip3-related mitophagy activity-dependent neuronal control neuroblastoma sh-sy5y cells membrane-targeted death ligand full article pdf bcl-xl regulates structure-mediated mitochondrial transfer 3-n-butylphthalide bearing article apoptosis aims astrocyte targeted overexpression martins de brito er-mitochondrial contact site vitro ischemia-reperfusion model cerebral oxygen consumption alpha-induced phosphorylation pink1 induces mitophagy mitochondrial permeability transition drp1 dependent manner nf-kappab signaling quality control axis proinflammatory microglial activation acute cerebral ischemia intrinsic mitochondrial pathway delayed neuronal damage astrocyte gap junctions

Questions {❓}

Bordt EA, Polster BM (2014) NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?
Dimmer KS, Scorrano L (2006) (De)constructing mitochondria: what for?
Rayasam A, Hsu M, Kijak JA, Kissel L, Hernandez G, Sandor M, Fabry Z (2018) Immune responses in stroke: how the immune system contributes to damage and healing after stroke and how this knowledge could be translated to better cures?
Song BD, Schmid SL (2003) A molecular motor or a regulator?

Schema {🗺️}

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         Reactive oxygen species
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         Cell Biology
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         general
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