CRM1 mediates ASC nuclear export and inflammasome activation DOI
Rui Cao, Bolong Lin,

Hongbin He

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 153, С. 114503 - 114503

Опубликована: Март 26, 2025

Язык: Английский

Metabolic reprogramming and polarization of microglia in Parkinson’s disease: Role of inflammasome and iron DOI
Haiyang Yu, Qing Chang,

Tong Sun

и другие.

Ageing Research Reviews, Год журнала: 2023, Номер 90, С. 102032 - 102032

Опубликована: Авг. 10, 2023

Язык: Английский

Процитировано

65

The role of mitochondrial dynamics in cerebral ischemia-reperfusion injury DOI Open Access
Jie Huang, Lei Chen,

Zi‐Meng Yao

и другие.

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

Inflammasomes in neurological disorders — mechanisms and therapeutic potential DOI
Kishore Aravind Ravichandran, Michael T. Heneka

Nature Reviews Neurology, Год журнала: 2024, Номер 20(2), С. 67 - 83

Опубликована: Янв. 9, 2024

Язык: Английский

Процитировано

40

Mitochondrial diseases: from molecular mechanisms to therapeutic advances DOI Creative Commons
Hu Wen,

Hui Deng,

Bingyan Li

и другие.

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

The Interplay between α-Synuclein and Microglia in α-Synucleinopathies DOI Open Access
Jacob Deyell, Manjari Sriparna, Mingyao Ying

и другие.

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

Focusing on mitochondria in the brain: from biology to therapeutics DOI Creative Commons

Nanshan Song,

Shuyuan Mei,

Xiang-Xu Wang

и другие.

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

Resveratrol protects against a high-fat diet-induced neuroinflammation by suppressing mitochondrial fission via targeting SIRT1/PGC-1α DOI
Xiaojuan Su, Qiong Li,

Mingzhi Yang

и другие.

Experimental Neurology, Год журнала: 2024, Номер 380, С. 114899 - 114899

Опубликована: Июль 24, 2024

Язык: Английский

Процитировано

8

From mitochondrial dysfunction to neuroinflammation in Parkinson’s disease: Pathogenesis and mitochondrial therapeutic approaches DOI
Negar Ebadpour, Mahmoud Mahmoudi, Ramiar Kamal Kheder

и другие.

International Immunopharmacology, Год журнала: 2024, Номер 142, С. 113015 - 113015

Опубликована: Сен. 1, 2024

Язык: Английский

Процитировано

7

Protective role of mitophagy on microglia-mediated neuroinflammatory injury through mtDNA-STING signaling in manganese-induced parkinsonism DOI Creative Commons
Lu Yang, Liang Gao, Yuqing Yang

и другие.

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

Research progress in the molecular mechanism of ferroptosis in Parkinson's disease and regulation by natural plant products DOI
Kailin Yang,

Liuting Zeng,

Jinsong Zeng

и другие.

Ageing Research Reviews, Год журнала: 2023, Номер 91, С. 102063 - 102063

Опубликована: Сен. 9, 2023

Язык: Английский

Процитировано

17