Journal of Molecular Graphics and Modelling, Journal Year: 2024, Volume and Issue: 128, P. 108702 - 108702
Published: Jan. 3, 2024
Language: Английский
Journal of Molecular Graphics and Modelling, Journal Year: 2024, Volume and Issue: 128, P. 108702 - 108702
Published: Jan. 3, 2024
Language: Английский
Nature reviews. Immunology, Journal Year: 2022, Volume and Issue: 23(3), P. 159 - 173
Published: July 25, 2022
Language: Английский
Citations
560Physiological Reviews, Journal Year: 2023, Volume and Issue: 103(4), P. 2349 - 2422
Published: April 6, 2023
Mitochondria are well known as organelles responsible for the maintenance of cellular bioenergetics through production ATP. Although oxidative phosphorylation may be their most important function, mitochondria also integral synthesis metabolic precursors, calcium regulation, reactive oxygen species, immune signaling, and apoptosis. Considering breadth responsibilities, fundamental metabolism homeostasis. Appreciating this significance, translational medicine has begun to investigate how mitochondrial dysfunction can represent a harbinger disease. In review, we provide detailed overview metabolism, bioenergetics, dynamics, autophagy, damage-associated molecular patterns, mitochondria-mediated cell death pathways, at any these levels is associated with disease pathogenesis. Mitochondria-dependent pathways thereby an attractive therapeutic target ameliorating human
Language: Английский
Citations
296Cell Metabolism, Journal Year: 2021, Volume and Issue: 33(9), P. 1853 - 1868.e11
Published: Aug. 20, 2021
Language: Английский
Citations
277Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)
Published: May 15, 2024
Abstract Mitochondria, with their intricate networks of functions and information processing, are pivotal in both health regulation disease progression. Particularly, mitochondrial dysfunctions identified many common pathologies, including cardiovascular diseases, neurodegeneration, metabolic syndrome, cancer. However, the multifaceted nature elusive phenotypic threshold dysfunction complicate our understanding contributions to diseases. Nonetheless, these complexities do not prevent mitochondria from being among most important therapeutic targets. In recent years, strategies targeting have continuously emerged transitioned clinical trials. Advanced intervention such as using healthy replenish or replace damaged mitochondria, has shown promise preclinical trials various Mitochondrial components, mtDNA, mitochondria-located microRNA, associated proteins can be potential agents augment function immunometabolic diseases tissue injuries. Here, we review current knowledge pathophysiology concrete examples We also summarize treat perspective dietary supplements targeted therapies, well translational situation related pharmacology agents. Finally, this discusses innovations applications transplantation an advanced promising treatment.
Language: Английский
Citations
239Nature Cell Biology, Journal Year: 2021, Volume and Issue: 23(12), P. 1271 - 1286
Published: Dec. 1, 2021
Language: Английский
Citations
186Theranostics, Journal Year: 2022, Volume and Issue: 12(6), P. 2928 - 2947
Published: Jan. 1, 2022
Rationale: Aberrant activation of macrophages with mitochondria dismiss was proved to be associated pathogenesis ALI (acute lung injury). Exosomes from adipose-derived mesenchymal stem cells (AdMSC-Exos) have been distinguished by their low immunogenicity, lack tumorigenicity, and high clinical safety, but role in treating the mechanism involved need defined. In this study, we sought investigate whether mitochondrial donation AdMSC-Exos provides profound protection against LPS-induced mice, accompanied improvement macrophage function. Methods: C57BL/6 mice were orotracheally instilled LPS (1 mg/kg). administered via tail vein 4 h after inhalation. Flow cytometry, H&E, Quantitative Real-Time PCR, immunofluorescence (IF), confocal microscopy imaging conducted tissue inflammation And further observe transfer exosomes effect on function MH-S through vitro experiments. Results: can cell-derived components alveolar a dose-dependent manner. Likely complementing damaged mitochondria, exhibited ability elevate level mtDNA, membrane potential (MMP), OXPHOS activity ATP generation, while reliving mROS stress LPS-challenged macrophages. Restoring integrity treatment enabled shifting anti-inflammatory phenotype, as featured down-regulation IL-1β, TNF-α iNOS secretion increase production cytokines IL-10 Arg-1. As depleted using clodronate liposomes, protective for largely abrogated. Conclusions: effectively donate component improved oxidative phosphorylation level, leading resumption metabolic immune homeostasis airway mitigating inflammatory pathology.
Language: Английский
Citations
182Cell Metabolism, Journal Year: 2022, Volume and Issue: 34(4), P. 533 - 548.e12
Published: March 18, 2022
Language: Английский
Citations
163Trends in Cell Biology, Journal Year: 2023, Volume and Issue: 34(2), P. 90 - 108
Published: July 27, 2023
Language: Английский
Citations
154Ageing Research Reviews, Journal Year: 2023, Volume and Issue: 88, P. 101955 - 101955
Published: May 15, 2023
Language: Английский
Citations
142Cells, Journal Year: 2021, Volume and Issue: 10(11), P. 2898 - 2898
Published: Oct. 26, 2021
Besides their role in cell metabolism, mitochondria display many other functions. Mitochondrial DNA (mtDNA), the own genome of organelle, plays an important modulating inflammatory immune response. When released from mitochondrion to cytosol, mtDNA is recognized by cGAS, a cGAMP which activates pathway leading enhanced expression type I interferons, and NLRP3 inflammasome, promotes activation pro-inflammatory cytokines Interleukin-1beta Interleukin-18. Furthermore, can be bound Toll-like receptor 9 endosome activate that ultimately leads cytokines. extracellular space different forms (free DNA, protein-bound fragments) either as free circulating molecules or encapsulated vesicles. In this review, we discussed latest findings concerning molecular mechanisms regulate release mitochondria, connect misplacement inflammation pathophysiological conditions.
Language: Английский
Citations
134