European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 968, P. 176368 - 176368
Published: Feb. 3, 2024
Language: Английский
Life Sciences, Journal Year: 2023, Volume and Issue: 334, P. 122257 - 122257
Published: Nov. 8, 2023
Language: Английский
Citations
44
International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(18), P. 13835 - 13835
Published: Sept. 8, 2023
Mitophagy is crucial for maintaining mitochondrial quality. However, its assessment in vivo challenging. The endosomal-lysosomal system a more accessible pathway through which subtypes of extracellular vesicles (EVs), also contain constituents, are released disposal. inclusion components into EVs occurs the setting mild damage and during impairment lysosomal function. By releasing mitochondrial-derived (MDVs), cells limit unload damage-associated molecular patterns with proinflammatory activity. Both positive negative effects on recipient have been described. Whether this due to production other than those containing mitochondria, such as MDVs, holding specific biological functions currently unknown. Evidence existence different MDV has produced. their characterization not always pursued, would be relevant exploring dynamics quality control health disease. Furthermore, classification may instrumental understanding roles promoting implementation biomarkers clinical studies.
Language: Английский
Citations
25
Acta Biomaterialia, Journal Year: 2023, Volume and Issue: 164, P. 1 - 14
Published: March 25, 2023
Language: Английский
Citations
24
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(4), P. 2052 - 2052
Published: Feb. 8, 2024
Sarcopenia, the age-associated decline in skeletal muscle mass and strength, is a condition with complex pathophysiology. Among factors underlying development of sarcopenia are progressive demise motor neurons, transition from fast to slow myosin isoform (type II type I fiber switch), decrease satellite cell number function. Mitochondrial dysfunction has been indicated as key contributor myocyte loss physical performance aging. Several systems have implicated regulation plasticity trophism such fine-tuned between stimulator protein synthesis, mechanistic target rapamycin (mTOR), inhibitor mTOR, AMP-activated kinase (AMPK), that promotes catabolism. Here, we provide an overview molecular mechanisms linking mitochondrial signaling quality homeostasis discuss main pathways elicited by their imbalance during age-related wasting. We also lifestyle interventions (i.e., exercise nutrition) may be exploited preserve function aged muscle. Finally, illustrate emerging possibility rescuing tissue through transplantation.
Language: Английский
Citations
12
Cells, Journal Year: 2024, Volume and Issue: 13(5), P. 410 - 410
Published: Feb. 27, 2024
Mitochondria, the energy suppliers of cells, play a central role in variety cellular processes essential for survival or leading to cell death. Consequently, mitochondrial dysfunction is implicated numerous general and CNS disorders. The clinical manifestations include metabolic disorders, immune system, tumorigenesis, neuronal behavioral abnormalities. In this review, we focus on CNS, which has unique characteristics therefore highly dependent mitochondria. First, review mitochondria development, synaptogenesis, plasticity, behavior as well their adaptation intricate connections between different types brain. Then, sparse knowledge mechanisms exogenous uptake describe attempts determine half-life transplantation long-term effects sprouting, proteome, behavior. We further discuss potential serve tool study causal link activity Next, transplantation’s therapeutic various Finally, basic reverse—translation challenges approach that currently hinder use transplantation.
Language: Английский
Citations
10
Biomolecules, Journal Year: 2024, Volume and Issue: 14(4), P. 415 - 415
Published: March 28, 2024
Sarcopenia has a complex pathophysiology that encompasses metabolic dysregulation and muscle ultrastructural changes. Among the drivers of intracellular changes fibers in sarcopenia, mitochondria their quality control pathways play relevant roles. Mononucleated stem cells/satellite cells (MSCs) have been attributed critical role repair after an injury. The involvement supporting MSC-directed is unclear. There evidence reduction mitochondrial biogenesis blunts repair, thus indicating delivery functional to injured muscles can be harnessed limit fibrosis enhance restoration function. Injection autologous respiration-competent from uninjured sites damaged tissue shown reduce infarct size cell survival preclinical models ischemia-reperfusion. Furthermore, incorporation donor into MSCs enhances lung cardiac repair. This strategy also tested for regeneration purposes traumatic injuries. Indeed, systemic promotes restores mass function while reducing during recovery In this review, we discuss contribution altered MSC sarcopenia illustrate prospect harnessing as therapeutic against age-related sarcopenia.
Language: Английский
Citations
9
Small, Journal Year: 2024, Volume and Issue: 20(29)
Published: Feb. 22, 2024
Parkinson's disease (PD) is currently the second most incurable central neurodegenerative resulting from various pathogenesis. As "energy factory" of cells, mitochondria play an extremely important role in supporting neuronal signal transmission and other physiological activities. Mitochondrial dysfunction can cause accelerate occurrence progression PD. How to effectively prevent suppress mitochondrial disorders a key strategy for treatment PD root. Therefore, emerging mitochondria-targeted therapy has attracted considerable interest. Herein, relationship between PD, causes results dysfunction, major strategies ameliorating treat are systematically reviewed. The study also prospects main challenges
Language: Английский
Citations
8
International Journal of Cardiology, Journal Year: 2024, Volume and Issue: 410, P. 132227 - 132227
Published: June 5, 2024
Language: Английский
Citations
8
ACS Nano, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 24, 2025
Mitochondrial transplantation is a significant therapeutic approach for addressing mitochondrial dysfunction in patients with spinal cord injury (SCI), yet it limited by rapid deactivation and low transfer efficiency. Here, high-quality mitochondria microfactories (HQ-Mitofactories) were constructed anchoring Prussian blue nanoenzymes onto mesenchymal stem cells effective to treat paralysis from SCI. Notably, the results demonstrated that HQ-Mitofactories could continuously produce vitality-boosting highly interconnected elongated network structures under oxidative stress scavenging excessive ROS. Furthermore, enabled efficient of injured neurons primarily via gap junctions, resulting restoration homeostasis thereby suppressing intracellular ROS burst facilitating neuronal repair. After i.v. administration, migrated cords SCI mice subsequently promoted regeneration remyelination. Consequently, HQ-Mitofactory-treated successfully recovered locomotor function within 4 weeks, 40% fully restoring walking after hindlimb paralysis. Conversely, untreated exhibited completely abolished movements. In light real-time generation even enabling targeted transfer, have promising potential context reduce SCI-related paralysis, more broadly impact field neuroregenerative medicine.
Language: Английский
Citations
1
Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)
Published: May 25, 2023
Abstract Cardiovascular disease (CVD) is the leading cause of noncommunicable disease-related death worldwide, and effective therapeutic strategies against CVD are urgently needed. Mitochondria dysfunction involves in onset development CVD. Nowadays, mitochondrial transplantation, an alternative treatment aimed at increasing number improving function, has been emerged with great potential. Substantial evidence indicates that transplantation improves cardiac function outcomes patients Therefore, profound implications prevention Here, we review abnormalities occur summarize for
Language: Английский
Citations
19