Biology, Год журнала: 2024, Номер 13(12), С. 1067 - 1067
Опубликована: Дек. 20, 2024
Most benthic marine invertebrates exhibit a characteristic biphasic life cycle, consisting of planktonic larval stage followed by adult [...]
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 95, С. 102233 - 102233
Опубликована: Фев. 14, 2024
Язык: Английский
Процитировано
17
Frontiers in Cell and Developmental Biology, Год журнала: 2025, Номер 12
Опубликована: Янв. 6, 2025
Graves disease (GD), an autoimmune affects the thyroid gland, results in hyperthyroidisms and goiter. The main cause of GD is not clearly defined; however, stimulating autoantibodies for hormone receptor (TSHR) known as thyroid-stimulating immunoglobulins (TSIs) are primary proposed mechanism. TSI activation TSHRs gland excessive release hormones with subsequent development hyperthyroidism cellular process macroautophagy/autophagy implicated pathogenesis other diseases. Autophagy plays a critical role many diseases different stages same through modulation immunity inflammatory response. In addition, autophagy also thyroid-associated ophthalmopathy (TAO). However, exact well explained. Therefore, this review discusses how intricately involved regarding its protective harmful effects.
Язык: Английский
Процитировано
2
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(8), С. 4161 - 4161
Опубликована: Апрель 9, 2024
Neuroinflammation and epilepsy are different pathologies, but, in some cases, they so closely related that the activation of one pathologies leads to development other. In this work, we discuss three main cell types involved neuroinflammation, namely (i) reactive astrocytes, (ii) activated microglia, infiltration (iii) peripheral immune cells central nervous system. Then, how neuroinflammation interconnected describe use repurposing drugs with anti-inflammatory properties have been shown a beneficial effect models. This review reinforces idea compounds designed alleviate seizures need target not only caused by astrocytes microglia but also interaction these infiltrated cells.
Язык: Английский
Процитировано
15
Diabetes Obesity and Metabolism, Год журнала: 2024, Номер 26(8), С. 3031 - 3044
Опубликована: Май 27, 2024
Abstract Depression is a mood disorder that may increase risk for the development of insulin resistance (IR) and type 2 diabetes (T2D), vice versa. However, mechanistic pathway linking depression T2D not fully elucidated. The aim this narrative review, therefore, was to discuss possible link between T2D. coexistence twice as great compared occurrence either condition independently. Hyperglycaemia dyslipidaemia promote incidence by enhancing inflammation reducing brain serotonin (5‐hydroxytryptamine [5HT]). Dysregulation signalling in impairs 5HT signalling, leading depression. Furthermore, associated with hyperglycaemia poor glycaemic control. Psychological stress In conclusion, could be potential factor through induction inflammatory reactions oxidative affect neurotransmission. addition, chronic induce dysregulation hypothalamic–pituitary–adrenal axis circulating cortisol levels, which triggers IR
Язык: Английский
Процитировано
12
Ageing Research Reviews, Год журнала: 2024, Номер 94, С. 102200 - 102200
Опубликована: Янв. 17, 2024
Язык: Английский
Процитировано
10
Autophagy, Год журнала: 2024, Номер unknown, С. 1 - 12
Опубликована: Июнь 14, 2024
Macroautophagy/autophagy is an essential degradation process that removes abnormal cellular components, maintains homeostasis within cells, and provides nutrition during starvation. Activated autophagy enhances cell survival stressful conditions, although overactivation of triggers induction autophagic death. Therefore, early-onset promotes whereas late-onset provokes programmed death, which can prevent disease progression. Moreover, regulates pancreatic β-cell functions by different mechanisms, the precise role in type 2 diabetes (T2D) not completely understood. Consequently, this mini-review discusses protective harmful roles β pathophysiology T2D.
Язык: Английский
Процитировано
8
Brain Research Bulletin, Год журнала: 2025, Номер 221, С. 111189 - 111189
Опубликована: Янв. 5, 2025
Epilepsy is a neurological disease characterized by unprovoked recurrent epileptic seizures. Temporal lobe epilepsy (TLE) the commonest type of focal in adults that resist to conventional anti-seizure medications (ASMs). Interestingly, ASMs do not affect epileptogenesis and progression disease. Therefore, repurposing natural products with anti-inflammatory, anti-oxidant effects such as berberine (BRB) may be logical treating refractory TLE. However, molecular mechanism BRB against development seizure mainly TLE was fully elucidated. we attempt this review discuss potential underlying
Язык: Английский
Процитировано
1
Cells, Год журнала: 2023, Номер 12(22), С. 2595 - 2595
Опубликована: Ноя. 9, 2023
Metabolic disorders and diabetes (DM) impact more than five hundred million individuals throughout the world are insidious in onset, chronic nature, yield significant disability death. Current therapies that address nutritional status, weight management, pharmacological options may delay but cannot alter disease course or functional organ loss, such as dementia degeneration of systemic bodily functions. Underlying these challenges onset aging associated with increased lifespan, telomere dysfunction, oxidative stress generation lead to multi-system dysfunction. These hurdles point urgent need underlying mechanisms innovative applications. New treatment strategies involve non-coding RNA pathways microRNAs (miRNAs) circular ribonucleic acids (circRNAs), Wnt signaling, Wnt1 inducible signaling pathway protein 1 (WISP1) dependent upon programmed cell death pathways, cellular metabolic AMP-activated kinase (AMPK) nicotinamide, growth factor Non-coding RNAs, AMPK cornerstone for overseeing complex offer avenues DM will necessitate continued appreciation ability each independently unison influence clinical outcome.
Язык: Английский
Процитировано
11
Frontiers in Cellular Neuroscience, Год журнала: 2025, Номер 18
Опубликована: Янв. 14, 2025
Protein lactylation is a new form of post-translational modification that has recently been proposed. Lactoyl groups, derived mainly from the glycolytic product lactate, have linked to protein in brain tissue, which shown correlate with increased neuronal excitability. Ischemic stroke may promote glycolysis, leading lactate accumulation tissue. This heighten excitability by upregulating levels, potentially triggering post-stroke epilepsy. Although current clinical treatments for seizures advanced significantly, approximately 30% patients epilepsy remain unresponsive medication, and prevalence continues rise. study explores mechanisms epilepsy-associated death mediated metabolism lactylation. also examines potential histone deacetylase inhibitors alleviate modifying thereby offering fresh perspectives future research into pathogenesis treatment
Язык: Английский
Процитировано
0
Frontiers in Neurology, Год журнала: 2025, Номер 15
Опубликована: Янв. 22, 2025
Background Epilepsy, a common neurological disorder, is characterized by susceptibility to recurrent seizures. Increasing evidence suggests that autophagy plays crucial role in the initiation and progression of epilepsy. However, precise mechanisms which deficiencies involved epileptogenesis are still not fully understood. Methods Two datasets epilepsy (GSE143272 GSE256068) were downloaded from Gene Expression Omnibus (GEO) database. Differential expression genes (DEGs) analysis weighted gene co-expression network (WGCNA) employed screen for related differential (ARDEGs) GSE143272 Subsequently, protein–protein interaction, transcription factors miRNAs networks constructed. Additionally, functional enrichment Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) applied. The hub ARDEGs identified through CytoHubba, followed LASSO analysis. Immune Cell Abundance Identifier (ImmuCellAI) was used estimate peripheral immune cells abundance Furthermore, level detected patients treated with different monotherapies explore responsiveness antiepileptic drug therapy. Finally, further validated hippocampus GSE256068 enhance reliability results. Results Twenty screened out integrating DEGs WGCNA KEGG showed only autophagy, but also apoptosis, NOD-like receptor signaling pathway, neurotrophin etc. Four (PIK3R1, TRIM21, TRIM22, ITPR3) CytoHubba plug infiltration there significantly increased macrophages decreased CD4 CD8 T cells, including Tr1, nTreg, Tfh, naïve, cytotoxic effector memory group. correlated cells. In validation anti-epileptic analysis, PIK3R1 ITPR3 had significant differences found be carbamazepine resistance. Conclusion This study elucidated autophagy-related signatures clarified their association responsiveness, providing novel target future therapeutic interventions disease markers
Язык: Английский
Процитировано
0