Cancer Letters, Год журнала: 2023, Номер 557, С. 216077 - 216077
Опубликована: Янв. 30, 2023
Язык: Английский
Cancer Letters, Год журнала: 2023, Номер 557, С. 216077 - 216077
Опубликована: Янв. 30, 2023
Язык: Английский
Biological Psychiatry, Год журнала: 2021, Номер 91(5), С. 449 - 458
Опубликована: Май 31, 2021
Язык: Английский
Процитировано
52Cells, Год журнала: 2021, Номер 10(5), С. 1009 - 1009
Опубликована: Апрель 24, 2021
The secondary injury process after traumatic brain (TBI) results in motor dysfunction, cognitive and emotional impairment, poor outcomes. These cascades include excitotoxic injury, mitochondrial oxidative stress, ion imbalance, inflammation, increased vascular permeability. Electron microscopy is an irreplaceable tool to understand the complex pathogenesis of TBI as usually accompanied by a series pathologic changes at ultra-micro level cells. ultrastructural different parts neurons (cell body, axon, synapses), glial cells, blood-brain barrier, etc. In view current difficulties treatment TBI, identifying subcellular structures can help us better cascade reactions improve clinical diagnosis treatment. purpose this review summarize discuss related (e.g., condensed membrane ferroptosis), barrier existing reports deepen in-depth study pathomechanism, hoping provide future research direction treatment, with ultimate aim improving prognosis patients TBI.
Язык: Английский
Процитировано
49Antioxidants and Redox Signaling, Год журнала: 2022, Номер 38(1-3), С. 234 - 257
Опубликована: Май 17, 2022
Significance: Autophagy and apoptosis are two important cellular mechanisms behind brain injuries, which severe clinical situations with increasing incidences worldwide. To search for more better treatments it is essential to deepen the understanding of autophagy, apoptosis, their interactions in injuries. This article first analyzes how autophagy participate pathogenetic processes injuries respectively mutually, then summarizes some promising targeting show potential applications personalized medicine precision future. Recent Advances: Most current studies suggest that detrimental recovery. Several indicate can cause unnecessary death neurons after while others beneficial acute (ABIs) by facilitating removal damaged proteins organelles. Whether or ABIs depends on many factors, results from different research groups diverse even controversial, making this topic appealing be explored further. Critical Issues: Neuronal primary pathological ABIs. How they interact each other regulations affect outcome prognosis remain uncertain, these answers critical. Future Directions: Insights into interplay between accurate balance may promote precise field Antioxid. Redox Signal. 38, 234–257.
Язык: Английский
Процитировано
32Advanced Science, Год журнала: 2023, Номер 10(20)
Опубликована: Апрель 27, 2023
Evidence suggests a unique association between bone aging and neurodegenerative/cerebrovascular disorders. However, the mechanisms underlying bone-brain interplay remain elusive. Here platelet-derived growth factor-BB (PDGF-BB) produced by preosteoclasts in is reported to promote age-associated hippocampal vascular impairment. Aberrantly elevated circulating PDGF-BB aged mice high-fat diet (HFD)-challenged correlates with capillary reduction, pericyte loss, increased blood-brain barrier (BBB) permeability their hippocampus. Preosteoclast-specific Pdgfb transgenic markedly high plasma concentration faithfully recapitulate BBB impairment cognitive decline. Conversely, preosteoclast-specific knockout have attenuated or HFD-challenged mice. Persistent exposure of brain pericytes concentrations upregulates matrix metalloproteinase 14 (MMP14), which promotes ectodomain shedding PDGF receptor β (PDGFRβ) from surface. MMP inhibitor treatment alleviates loss reduction conditional antagonizes leakage The findings establish role bone-derived mediating disruption identify ligand-induced PDGFRβ as feedback mechanism for downregulation consequent loss.
Язык: Английский
Процитировано
22Cancer Letters, Год журнала: 2023, Номер 557, С. 216077 - 216077
Опубликована: Янв. 30, 2023
Язык: Английский
Процитировано
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