Mitochondria targeting drugs for neurodegenerative diseases—Design, mechanism and application

Xu, Jiajia; Du, Yong; Zhao, Yunhe; Lim, Kah‐Leong; Lü, Li; Zhang, Chengwu; Li, Lin

doi:10.1016/j.apsb.2022.03.001

Cited by 47 publications

(29 citation statements)

References 99 publications

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“…The results show that the activity of intracellular CAT was effectively suppressed after CaS@PP and I-CaS@PP treatments due to the generated H 2 S, which would be further inhibited with exposure to laser irradiation, proving that ICG-mediated thermal energy stimulated H 2 S production. It is well known that CAT is an antioxidant enzyme overexpressed in tumor cells that catalyzes H 2 O 2 into water and oxygen, which influences cancer progression and strengthens resistance to various therapies 36 , 37 , 38 , 39 , 40 , 41 , 42 . Therefore, the decrease of CAT activity affected by H 2 S may contribute to inhibit the decomposition of harmful substance H 2 O 2 and elevate intracellular oxidative stress 16 .…”

Section: Resultsmentioning

confidence: 99%

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Lin

Huang

Shi

et al. 2022

Acta Pharmaceutica Sinica B

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Section: Resultsmentioning

confidence: 99%

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Lin

Huang

Shi

et al. 2022

Acta Pharmaceutica Sinica B

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“…[ 54 ] TPP + ‐conjugated molecules, such as mitoQ, Mito‐Apocynin, and Mito‐SOD, have been applied for the treatment of PD in the clinic. [ 55,56 ] Based on the above research, we designed and synthesized three TPP‐conjugated VB 3 derivatives to assess their neuroprotective efficacy. Nevertheless, some studies have established that the TPP + moiety has detrimental effects on mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial‐Targeting Vitamin B₃ Ameliorates the Phenotypes of Parkinson's Disease In Vitro and In Vivo by Restoring Mitochondrial Function

Xin

Yang

Ding

et al. 2022

Advanced Therapeutics

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Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by progressive dopaminergic neuron loss, which affects millions of people worldwide, especially elderly individuals. Mitochondrial dysfunction is believed to be one crucial causative factor of PD. Therefore, restoring mitochondrial function is highly recommended for the treatment of PD. Herein, it is found that vitamin B 3 (VB 3 ) protects the dopaminergic cell line SH-SY5Y against rotenone-induced apoptosis by restoring mitochondrial dysfunction. To further improve the efficacy, a derivative of VB 3 , mitochondrial-targeting VB 3 (Mito-VB 3 ), is developed. It is demonstrated that Mito-VB 3 rescues SH-SY5Y cells from the neurotoxicity of oxidative stress. More importantly, Mito-VB 3 ameliorates the phenotypes of the Drosophila PD model. Mechanistically, Mito-VB 3 enhances nicotinamide adenine dinucleotide (NAD + ) levels, reduces ROS generation, elevates ATP levels, and restores mitochondrial membrane potential. Meanwhile, Mito-VB 3 promotes mitochondrial biogenesis by activating the NAD + /SIRT1/PGC1𝜶 pathway. In summary, the results demonstrate that Mito-VB 3 displays remarkable neuroprotective effects in the cell and Drosophila PD models and that Mito-VB 3 might serve as a potential therapeutic candidate for the treatment of PD and other mitochondrial dysfunction-related diseases.

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“…The challenge is to develop a strategy to deliver a drug to mitochondria in specific cell types. Possibly, encapsulation of drugs/mitochondria into nanolipidic carriers may overcome these challenges (321)(322)(323)(324) and allow the use of mitochondria/mitochondria targeting drugs to treat pain. As an example, in a pre-clinical study, extracellular vesicle containing mitochondria resolved persistent inflammatory pain, albeit transiently (25).…”

Section: Mitochondrial Transfer/transplantationmentioning

confidence: 99%

Mitochondria and sensory processing in inflammatory and neuropathic pain

2022

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Rheumatic diseases, such as osteoarthritis and rheumatoid arthritis, affect over 750 million people worldwide and contribute to approximately 40% of chronic pain cases. Inflammation and tissue damage contribute to pain in rheumatic diseases, but pain often persists even when inflammation/damage is resolved. Mechanisms that cause this persistent pain are still unclear. Mitochondria are essential for a myriad of cellular processes and regulate neuronal functions. Mitochondrial dysfunction has been implicated in multiple neurological disorders, but its role in sensory processing and pain in rheumatic diseases is relatively unexplored. This review provides a comprehensive understanding of how mitochondrial dysfunction connects inflammation and damage-associated pathways to neuronal sensitization and persistent pain. To provide an overall framework on how mitochondria control pain, we explored recent evidence in inflammatory and neuropathic pain conditions. Mitochondria have intrinsic quality control mechanisms to prevent functional deficits and cellular damage. We will discuss the link between neuronal activity, mitochondrial dysfunction and chronic pain. Lastly, pharmacological strategies aimed at reestablishing mitochondrial functions or boosting mitochondrial dynamics as therapeutic interventions for chronic pain are discussed. The evidence presented in this review shows that mitochondria dysfunction may play a role in rheumatic pain. The dysfunction is not restricted to neuronal cells in the peripheral and central nervous system, but also includes blood cells and cells at the joint level that may affect pain pathways indirectly. Pre-clinical and clinical data suggest that modulation of mitochondrial functions can be used to attenuate or eliminate pain, which could be beneficial for multiple rheumatic diseases.

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Mitochondria targeting drugs for neurodegenerative diseases—Design, mechanism and application

Cited by 47 publications

References 99 publications

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Mitochondrial‐Targeting Vitamin B₃ Ameliorates the Phenotypes of Parkinson's Disease In Vitro and In Vivo by Restoring Mitochondrial Function

Mitochondria and sensory processing in inflammatory and neuropathic pain

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Mitochondria targeting drugs for neurodegenerative diseases—Design, mechanism and application

Cited by 47 publications

References 99 publications

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Biodegradable calcium sulfide-based nanomodulators for H2S-boosted Ca2+-involved synergistic cascade cancer therapy

Mitochondrial‐Targeting Vitamin B3 Ameliorates the Phenotypes of Parkinson's Disease In Vitro and In Vivo by Restoring Mitochondrial Function

Mitochondria and sensory processing in inflammatory and neuropathic pain

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Mitochondrial‐Targeting Vitamin B₃ Ameliorates the Phenotypes of Parkinson's Disease In Vitro and In Vivo by Restoring Mitochondrial Function