ACS Central Science, Год журнала: 2025, Номер unknown
Опубликована: Апрель 13, 2025
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 95, С. 102233 - 102233
Опубликована: Фев. 14, 2024
Язык: Английский
Процитировано
18
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
Ageing Research Reviews, Год журнала: 2023, Номер 91, С. 102084 - 102084
Опубликована: Окт. 5, 2023
Язык: Английский
Процитировано
32
Journal of Cellular and Molecular Medicine, Год журнала: 2024, Номер 28(10)
Опубликована: Май 1, 2024
Parkinson's disease (PD) is a neurodegenerative disorder of the brain and manifested by motor non-motor symptoms because degenerative changes in dopaminergic neurons substantia nigra. PD neuropathology associated with mitochondrial dysfunction, oxidative damage apoptosis. Thus, modulation apoptosis growth factors could be novel boulevard management PD. Brain-derived neurotrophic factor (BDNF) its receptor tropomyosin kinase type B (TrkB) are chiefly involved neuropathology. BDNF promotes survival nigra enhances functional activity striatal neurons. Deficiency TrkB triggers degeneration accumulation α-Syn As well, BDNF/TrkB signalling reduced early phase Targeting specific activators may attenuate this review aimed to discuss potential role against In conclusion, decreased linked severity long-term complications. Activation
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
Autophagy, Год журнала: 2024, Номер 20(7), С. 1473 - 1482
Опубликована: Фев. 12, 2024
Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ) that results from autoantibodies against nicotinic acetylcholine receptors (nAchRs) at NMJs. These are mainly originated autoreactive B cells bind and destroy nAchRs NMJs preventing nerve impulses activating end-plates skeletal muscle. Indeed, immune dysregulation plays a crucial role in pathogenesis MG. Autoreactive increased MG due to defect central peripheral tolerance mechanisms. As well, T augmented diversion regulatory (T
Язык: Английский
Процитировано
11
Molecular Neurobiology, Год журнала: 2024, Номер 61(9), С. 7092 - 7108
Опубликована: Фев. 17, 2024
Abstract Parkinson’s disease (PD) is a progressive neurodegenerative of the brain due to degeneration dopaminergic neurons in substantia nigra (SN). Glycogen synthase kinase 3 beta (GSK-3β) implicated pathogenesis PD. Therefore, purpose present review was revise mechanistic role GSK-3β PD neuropathology, and how inhibitors affect neuropathology. GSK-3 conserved threonine/serine protein that intricate regulation cellular anabolic catabolic pathways by modulating glycogen synthase. Over-expression also interconnected with development different diseases. However, underlying mechanism neuropathology not fully clarified. induces triggering mitochondrial dysfunction oxidative stress SN. NF-κB NLRP3 inflammasome are activated response dysregulated leading neuronal injury. Higher expression early stages might contribute reduction neuroprotective brain-derived neurotrophic factor (BDNF). Thus, may be effective reducing inflammatory disorders which associated
Язык: Английский
Процитировано
11
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
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(18), С. 9947 - 9947
Опубликована: Сен. 15, 2024
Programmed cell death (PCD) is a form of distinct from accidental (ACD) and also referred to as regulated (RCD). Typically, PCD signaling events are precisely by various biomolecules in both spatial temporal contexts promote neuronal development, establish neural architecture, shape the central nervous system (CNS), although role extends beyond CNS. Abnormalities cascades contribute irreversible loss cells function, leading onset progression neurodegenerative diseases. In this review, we summarize molecular processes features different modalities PCD, including apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, other novel forms their effects on pathogenesis diseases, such Alzheimer’s disease (AD), Parkinson’s (PD), Huntington’s (HD), amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA), multiple (MS), traumatic brain injury (TBI), stroke. Additionally, examine key factors involved these pathways discuss potential for development therapeutic targets strategies. Therefore, strategies targeting inhibition or facilitation offer promising approach clinical applications treating
Язык: Английский
Процитировано
8