Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2022, Номер 395(12), С. 1463 - 1475
Опубликована: Сен. 5, 2022
Язык: Английский
Virology Journal, Год журнала: 2022, Номер 19(1)
Опубликована: Окт. 9, 2022
Most COVID-19 patients recovered with low mortality; however, some experienced long-term symptoms described as "long-COVID" or "Post-COVID syndrome" (PCS). Patients may have persisting for weeks after acute SARS-CoV-2 infection, including dyspnea, fatigue, myalgia, insomnia, cognitive and olfactory disorders. These last months in patients. PCS progress association the development of mast cell activation syndrome (MCAS), which is a distinct kind disorder, characterized by hyper-activation cells inappropriate excessive release chemical mediators. survivors, mainly women, persistent severe fatigue 10 recovery history neuropsychiatric disorders are more prone to develop PCS. High D-dimer levels blood urea nitrogen were observed be risk factors associated pulmonary dysfunction survivors 3 post-hospital discharge has systemic manifestations that resolve time no further complications. However, final outcomes chiefly unknown. Persistence inflammatory reactions, autoimmune mimicry, reactivation pathogens together host microbiome alterations contribute The deregulated mediators MCAS produces extraordinary during course infection correlated severity Therefore, treated antihistamines, inhibition synthesis mediators, mediator release, degranulation cells.
Язык: Английский
Процитировано
93
Frontiers in Microbiology, Год журнала: 2023, Номер 13
Опубликована: Янв. 13, 2023
Coronaviruses can cause serious respiratory tract infections and may also impact other end organs such as the central nervous system, lung heart. The coronavirus disease 2019 (COVID-19) has had a devastating on humanity. Understanding mechanisms that contribute to pathogenesis of infections, will set foundation for development new treatments attenuate with coronaviruses host cells tissues. During infection cells, trigger an imbalance between increased production reactive oxygen species (ROS) reduced antioxidant responses leads redox stress. Subsequently, stress contributes antiviral virus-induced inflammation apoptosis ultimately drive cell tissue damage organ disease. However, there is limited understanding how different including SARS-CoV-2, manipulate cellular machinery drives responses. This review aims elucidate involved in replication associated inflammation, apoptotic pathways, autoimmunity, vascular dysfunction collectively multiorgan damage.
Язык: Английский
Процитировано
62
Cellular and Molecular Neurobiology, Год журнала: 2023, Номер 43(6), С. 2743 - 2759
Опубликована: Апрель 19, 2023
Abstract Parkinson’s disease (PD) is one of the most common degenerative brain disorders caused by loss dopaminergic neurons in substantia nigra (SN). Lewy bodies and -synuclein accumulation SN are hallmarks neuropathology PD. Due to lifestyle changes prolonged L-dopa administration, patients with PD frequently have vitamin deficiencies, especially folate, B6, B12. These augment circulating levels Homocysteine development hyperhomocysteinemia, which may contribute pathogenesis Therefore, this review aimed ascertain if hyperhomocysteinemia play a part oxidative inflammatory signaling pathways that development. Hyperhomocysteinemia implicated neurodegenerative disorders, including triggers progression different mechanisms, stress, mitochondrial dysfunction, apoptosis, endothelial dysfunction. Particularly, linked high systemic disorders. induces immune activation stress. In turn, activated response promotes hyperhomocysteinemia. hyperhomocysteinemia-induced immunoinflammatory abnormal aggravate PD, leading more severity. Also, like nuclear factor kappa B (NF-κB) nod-like receptor pyrin 3 (NLRP3) inflammasome other intricate conclusion, involved either directly via induction degeneration or indirectly pathways.
Язык: Английский
Процитировано
36
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
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
10
Inflammopharmacology, Год журнала: 2022, Номер 31(1), С. 1 - 7
Опубликована: Ноя. 23, 2022
Abstract In coronavirus disease 2019 (Covid-19) era, neuroinflammation may develop due to neuronal tropism of severe acute respiratory syndrome type 2 (SARS-CoV-2) and/or associated immune activation, cytokine storm, and psychological stress. SARS-CoV-2 infection linked storm cause blood–brain barrier (BBB) injury through which activated cells can pass into the brain causing activation glial with subsequent neuroinflammation. Different therapeutic regimens were suggested alleviate Covid-19-induced Since glibenclamide has anti-inflammatory neuroprotective effects, it could be effective in mitigation infection-induced Glibenclamide is a second-generation drug from sulfonylurea family, acts by inhibiting adenosine triphosphate (ATP)-sensitive K channel regulatory subunit 1 receptor (SUR-1) pancreatic β cells. reduces BBB nod-like pyrin 3 (NLRP3) inflammasome, oxidative stress, microglial activation. Therefore, inhibition NLRP3 stress attenuate SARS-CoV-2-mediated
Язык: Английский
Процитировано
37
Inflammopharmacology, Год журнала: 2022, Номер 30(5), С. 1493 - 1501
Опубликована: Авг. 3, 2022
Язык: Английский
Процитировано
30
CNS Neuroscience & Therapeutics, Год журнала: 2023, Номер 30(4)
Опубликована: Ноя. 12, 2023
Abstract Depression is a mood disorder characterized by abnormal thoughts. The pathophysiology of depression related to the deficiency serotonin (5HT), which derived from tryptophan (Trp). Mitochondrial dysfunction, oxidative stress, and neuroinflammation are involved in pathogenesis depression. Notably, renin–angiotensin system (RAS) depression, different findings revealed that angiotensin‐converting enzyme inhibitors (ACEIs) angiotensin receptor blockers (ARBs) may be effective However, underlying mechanism for role dysregulated brain RAS‐induced remains speculative. Therefore, this review aimed revise conceivable ACEIs ARBs how these agents ameliorate Dysregulation RAS triggers development progression through reduction 5HT expression brain‐derived neurotrophic factor (BDNF) induction mitochondrial neuroinflammation. inhibition central classical ARBS activation non‐classical prevent regulating 5HT, BDNF,
Язык: Английский
Процитировано
17
Journal of Cellular and Molecular Medicine, Год журнала: 2024, Номер 28(12)
Опубликована: Июнь 1, 2024
Abstract Parkinson disease (PD) is one of the most common neurodegenerative diseases brain. Of note, brain renin‐angiotensin system (RAS) intricate in PD neuropathology through modulation oxidative stress, mitochondrial dysfunction and neuroinflammation. Therefore, RAS by angiotensin receptor blockers (ARBs) angiotensin‐converting enzyme inhibitors (ACEIs) may be effective reducing risk neuropathology. It has been shown that all components including peptides enzymes are present different areas. Brain plays a critical role regulation memory cognitive function, controlling central blood pressure. However, exaggerated implicated pathogenesis PD. Two well‐known pathways recognized including; classical pathway which mainly mediated AngII/AT1R detrimental effects. Conversely, non‐classical mostly ACE2/Ang1‐7/MASR AngII/AT2R beneficial effects against Exaggerated affects viability dopaminergic neurons. fundamental mechanism was not fully elucidated. Consequently, purpose this review to disclose mechanistic In addition, we try revise how ACEIs ARBs can developed for therapeutics
Язык: Английский
Процитировано
6
Frontiers in Pharmacology, Год журнала: 2022, Номер 13
Опубликована: Апрель 26, 2022
A novel severe acute respiratory distress syndrome coronavirus type 2 (SARS-CoV-2) has been confirmed as the cause of global pandemic disease 2019 (COVID-19). Different repurposed drugs have trialed and used in management COVID-19. One these agents was anti-cancer Selinexor (SXR). SXR is an drug that acts by inhibition nuclear exportin-1 (XPO1), which inhibits transport proteins from nucleus to cytoplasm, leading induction cell-cycle arrest apoptosis. XPO1 inhibitors had antiviral effects, mainly against syncytial virus (RSV) influenza virus. SARS-CoV-2 cytoplasm with further proliferation. ability prevent development a cytokine storm COVID-19 inhibiting release pro-inflammatory cytokines augmentation anti-inflammatory cytokines. In conclusion, infection linked activation XPO1, triggering inflammatory reactions oxidative stress. Inhibition (SXR), selective inhibitor export (SINE), can reduce proliferation associated disorders. Preclinical clinical studies are warranted this regard.
Язык: Английский
Процитировано
24