International Immunopharmacology, Год журнала: 2025, Номер 153, С. 114503 - 114503
Опубликована: Март 26, 2025
Язык: Английский
Ageing Research Reviews, Год журнала: 2023, Номер 90, С. 102032 - 102032
Опубликована: Авг. 10, 2023
Язык: Английский
Процитировано
65
Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 162, С. 114671 - 114671
Опубликована: Апрель 8, 2023
Stroke is one of the leading causes death and long-term disability worldwide. More than 80 % strokes are ischemic, caused by an occlusion cerebral arteries. Without question, restoration blood supply as soon possible first therapeutic strategy. Nonetheless paradoxically, reperfusion can further aggravate injury through a series reactions known ischemia-reperfusion (CIRI). Mitochondria play vital role in promoting nerve survival neurological function recovery mitochondrial dysfunction considered characteristics CIRI. Neurons often die due to oxidative stress imbalance energy metabolism following CIRI, there strong association with dysfunction. Altered dynamics reaction stress. Mitochondrial refers maintenance integrity, distribution, size mitochondria well their ability resist external stimuli continuous cycle fission fusion. Therefore, improving means treating This review discusses relationship between CIRI emphasizes potential approach improve prognosis
Язык: Английский
Процитировано
44
Nature Reviews Neurology, Год журнала: 2024, Номер 20(2), С. 67 - 83
Опубликована: Янв. 9, 2024
Язык: Английский
Процитировано
40
Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)
Опубликована: Янв. 9, 2025
Abstract Mitochondria are essential for cellular function and viability, serving as central hubs of metabolism signaling. They possess various metabolic quality control mechanisms crucial maintaining normal activities. Mitochondrial genetic disorders can arise from a wide range mutations in either mitochondrial or nuclear DNA, which encode proteins other contents. These defects lead to breakdown metabolism, such the collapse oxidative phosphorylation, one mitochondria’s most critical functions. diseases, common group disorders, characterized by significant phenotypic heterogeneity. Clinical symptoms manifest systems organs throughout body, with differing degrees forms severity. The complexity relationship between mitochondria diseases results an inadequate understanding genotype-phenotype correlation these historically making diagnosis treatment challenging often leading unsatisfactory clinical outcomes. However, recent advancements research technology have significantly improved our management conditions. translations mitochondria-related therapies actively progressing. This review focuses on physiological mitochondria, pathogenesis potential diagnostic therapeutic applications. Additionally, this discusses future perspectives diseases.
Язык: Английский
Процитировано
7
International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(3), С. 2477 - 2477
Опубликована: Янв. 27, 2023
Synucleinopathies are a set of devastating neurodegenerative diseases that share pathologic accumulation the protein α-synuclein (α-syn). This causes neuronal death resulting in irreversible dementia, deteriorating motor symptoms, and cognitive decline. While etiology these conditions remains largely unknown, microglia, resident immune cells central nervous system (CNS), have been consistently implicated pathogenesis synucleinopathies. Microglia generally believed to be neuroprotective early stages α-syn contribute further neurodegeneration chronic disease states. molecular mechanisms by which microglia achieve this role still being investigated, here we highlight major findings date. In review, describe how structural varieties inherently disordered result varied microglial receptor-mediated interactions. We also summarize receptors enable cellular recognition uptake α-syn. Lastly, review downstream effects processing within including spread other brain regions neuroinflammation Understanding mechanism interactions with is vital conceptualizing targets for novel therapeutic interventions. addition, given significant diversity pathophysiology synucleinopathies, such gauging all potential pathways state.
Язык: Английский
Процитировано
33
Translational Neurodegeneration, Год журнала: 2024, Номер 13(1)
Опубликована: Апрель 17, 2024
Abstract Mitochondria have multiple functions such as supplying energy, regulating the redox status, and producing proteins encoded by an independent genome. They are closely related to physiology pathology of many organs tissues, among which brain is particularly prominent. The demands 20% resting metabolic rate holds highly active mitochondrial activities. Considerable research shows that mitochondria function, while defects induce or exacerbate in brain. In this review, we provide comprehensive advances biology involved functions, well mitochondria-dependent cellular events pathology. Furthermore, various perspectives explored better identify roles neurological diseases neurophenotypes diseases. Finally, therapies discussed. Mitochondrial-targeting therapeutics showing great potentials treatment
Язык: Английский
Процитировано
17
Experimental Neurology, Год журнала: 2024, Номер 380, С. 114899 - 114899
Опубликована: Июль 24, 2024
Язык: Английский
Процитировано
8
International Immunopharmacology, Год журнала: 2024, Номер 142, С. 113015 - 113015
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
7
Journal of Neuroinflammation, Год журнала: 2025, Номер 22(1)
Опубликована: Фев. 28, 2025
Manganese (Mn), the third most abundant transition metal in earth's crust, has widespread applications emerging field of organometallic catalysis and traditional industries. Excessive Mn exposure causes neurological syndrome resembling Parkinson's disease (PD). The pathogenesis PD is thought to involve microglia-mediated neuroinflammatory injury, with mitochondrial dysfunction playing a role aberrant microglial activation. In early stages PD, PINK1/Parkin-mediated mitophagy contributes inflammatory response via cGAS/STING signaling pathway. Suppression due excessive exacerbates neuronal injury. Moreover, leads damage cGAS-STING However, precise modulating neuroinflammation Mn-induced parkinsonism its underlying molecular mechanism remains unclear. Here, we observed that Mn-exposed mice exhibited neurobehavioral abnormalities detrimental activation, along increased apoptosis nerve cells, proinflammatory cytokines, intracellular ROS. Furthermore, vivo vitro experiments showed resulted dysfunction, manifested by ROS, decreased mass, membrane potential. Additionally, escalating dose, changed from activation suppression. This was evidenced levels LC3-II, PINK1, p-Parkin/Parkin, p62 protein expression level, as well colocalization between ATPB LC3B exposure. Upregulation urolithin A could mitigate indicated potential, improvements deficits attenuated Using single-nucleus RNA-sequencing (snRNA-seq) analysis mouse model, identified pathway potential neuroinflammation. associated an increase cytosolic mtDNA levels, which activate STING signaling. These findings point induction viable strategy alleviate through mtDNA-STING
Язык: Английский
Процитировано
1
Ageing Research Reviews, Год журнала: 2023, Номер 91, С. 102063 - 102063
Опубликована: Сен. 9, 2023
Язык: Английский
Процитировано
17