Neurotoxicity Research, Journal Year: 2023, Volume and Issue: 41(1), P. 29 - 40
Published: Jan. 3, 2023
Language: Английский
Neurotoxicity Research, Journal Year: 2023, Volume and Issue: 41(1), P. 29 - 40
Published: Jan. 3, 2023
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(2), P. 993 - 993
Published: Jan. 12, 2024
Regenerative medicine harnesses the body's innate capacity for self-repair to restore malfunctioning tissues and organs. Stem cell therapies represent a key regenerative strategy, but effectively harness their potential necessitates nuanced understanding of stem niche. This specialized microenvironment regulates critical behaviors including quiescence, activation, differentiation, homing. Emerging research reveals that dysfunction within endogenous neural niches contributes neurodegenerative pathologies impedes regeneration. Strategies such as modifying signaling pathways, or epigenetic interventions niche homeostasis signaling, hold promise revitalizing neurogenesis repair in diseases like Alzheimer's Parkinson's. Comparative studies highly species provide evolutionary clues into niche-mediated renewal mechanisms. Leveraging bioelectric cues crosstalk between gut, brain, vascular further illuminates promising therapeutic opportunities. techniques single-cell transcriptomics, organoids, microfluidics, artificial intelligence, silico modeling, transdifferentiation will continue unravel complexity. By providing comprehensive synthesis integrating diverse views on components, developmental transitions, dynamics, this review unveils new layers complexity integral behavior function, which unveil novel prospects modulate function revolutionary treatments diseases.
Language: Английский
Citations
17Phytomedicine, Journal Year: 2025, Volume and Issue: 138, P. 156387 - 156387
Published: Jan. 12, 2025
Language: Английский
Citations
1Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)
Published: Jan. 28, 2025
The central nervous system (CNS) requires specialized blood vessels to support neural function within specific microenvironments. During neurovascular development, endothelial Wnt/β-catenin signaling is required for BBB development the brain parenchyma, whereas fenestrated that lack properties do not require signaling. Here, we used zebrafish further characterize this phenotypic heterogeneity of CNS vasculature. Using transgenic reporters transcriptional activity, found an inverse correlation between activated in cells (ECs) versus non-ECs these distinct Our results indicated level may regulate activity adjacent ECs. To test concept, generated a Tet-On inducible drive constitutively active β-catenin expression progenitor (NPCs). We dose-dependent activation NPCs caused severe deficiency angiogenesis and development. Additionally, discovered significant increase proliferation microglia infiltration peripheral neutrophils indicative stereotypical neuroinflammatory response. In conclusion, our demonstrate importance proper microenvironments highlights potentially deleterious consequences aberrant Wnt activation.
Language: Английский
Citations
1Communications Biology, Journal Year: 2025, Volume and Issue: 8(1)
Published: Feb. 11, 2025
Hypoxic postconditioning (HPC) was reported to stabilize nuclear β-catenin by inhibiting lysine (K)-specific demethylase 2 A (KDM2A) in hippocampal CA1 against transient global cerebral ischemia (tGCI). Herein we investigate how HPC inhibits the K48-linked poly-ubiquitination (K48-Ub)-related degradation of after tGCI. We confirmed that SCFKDM2A complex targets for via ubiquitin proteasome pathway vitro. reduced and K48-Ub β-catenin, increased ubiquitin-specific peptidase 22 (USP22) nucleus Furthermore, KDM2A knockdown decreased β-catenin-SCFKDM2A interaction Moreover, suppressed survivin expression attenuated neuroprotection induced HPC. In contrast, overexpression USP22 promoted deubiquitination enhanced neuroprotective effects offered Taken together, this study supports downregulated through suppressing increasing USP22, thereby inducing ischemic tolerance. The co-effects hypoxic on significantly hindered pathway, leading stabilization
Language: Английский
Citations
1International Journal of Cell Biology, Journal Year: 2023, Volume and Issue: 2023, P. 1 - 13
Published: Sept. 21, 2023
Defective Wnt signaling is found to be associated with various neurodegenerative diseases. In the canonical pathway, Frizzled receptor (Fzd) and lipoprotein receptor-related proteins 5/6 (LRP5/LRP6) create a seven-pass transmembrane complex which ligands bind. This interaction causes tumor suppressor adenomatous polyposis coli gene product (APC), casein kinase 1 (CK1), GSK-3β (glycogen synthase kinase-3 beta) recruited by scaffold protein Dishevelled (Dvl), in turn deactivates β-catenin destruction complex. inactivation stops from phosphorylating β-catenin. As result, first builds up cytoplasm then migrates into nucleus, where it binds Lef/Tcf transcription factor activate of more than 50 target genes, including those involved cell growth, survival, differentiation, neurogenesis, inflammation. The treatments that are currently available for illnesses most commonly not curative nature but only symptomatic. According all research, restoring Wnt/β-catenin brains patients disorders, particularly Alzheimer’s Parkinson’s disease, would improve condition several neurological disorders. importance activators modulators such mainly restore rather overstimulate signaling, thereby reestablishing equilibrium between Wnt-OFF Wnt-ON states. this review, we have tried summarize significance pathway pathophysiology certain diseases, as cerebral ischemia, Huntington’s multiple sclerosis, other similar how can restored these patients.
Language: Английский
Citations
21Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 101, P. 102536 - 102536
Published: Oct. 9, 2024
Language: Английский
Citations
6Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: Sept. 23, 2024
Language: Английский
Citations
5Neurochemical Research, Journal Year: 2023, Volume and Issue: 48(7), P. 1997 - 2016
Published: Feb. 14, 2023
Language: Английский
Citations
11Pharmacological Reports, Journal Year: 2023, Volume and Issue: 75(4), P. 838 - 860
Published: June 22, 2023
Language: Английский
Citations
11Scientific Reports, Journal Year: 2023, Volume and Issue: 13(1)
Published: Dec. 7, 2023
This study aimed to investigate the relationship between hypertension and Alzheimer's disease (AD) demonstrate key role of stroke in this using mediating Mendelian randomization. AD, a neurodegenerative characterized by memory loss, cognitive impairment, behavioral abnormalities, severely affects quality life patients. Hypertension is an important risk factor for AD. However, precise mechanism underlying unclear. To we used mediated randomization method screened variables AD setting instrumental variables. The results analysis showed that stroke, as variable, plays causal Specifically, indirect effect value obtained multivariate MR was 54.9%. implies approximately 55% owing can be attributed stroke. suggest increased through finding not only sheds light on but also indicates novel methods prevention treatment By identifying critical link provides insights into potential interventions could mitigate impact help develop personalized treatments improve patients with who suffer from hypertension.
Language: Английский
Citations
11