Ferroptosis in Parkinson’s disease: glia–neuron crosstalk

Wang, Zhangli; Yuan, Lin; Li, Wen; Li, Jia Yi

doi:10.1016/j.molmed.2022.02.003

Cited by 149 publications

(106 citation statements)

References 102 publications

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“…Recent studies on aging-related diseases have indicated that ferroptosis contributes in the pathogenesis of Alzheimer's disease (230-232), Parkinson's disease (233,234), Huntington's disease (235), Depression (236-238), Osteoarthritis (239), Myocardial ischemia and reperfusion (MI/R) (240)(241)(242), Atherosclerosis (243, 244), and Diabetes (245,246). Notably, quercetin shows iron-chelating activity and effectively decrease iron deposition in the hearts, kidneys and liver of iron-dextran-overloaded mice (247), and protects bone marrow-derived mesenchymal stem cells from erastin-induced ferroptosis through antioxidant pathway (248).…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

et al. 2022

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Quercetin, a naturally non-toxic flavonoid within the safe dose range with antioxidant, anti-apoptotic and anti-inflammatory properties, plays an important role in the treatment of aging-related diseases. Sirtuin 1 (SIRT1), a member of NAD+-dependent deacetylase enzyme family, is extensively explored as a potential therapeutic target for attenuating aging-induced disorders. SIRT1 possess beneficial effects against aging-related diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Depression, Osteoporosis, Myocardial ischemia (M/I) and reperfusion (MI/R), Atherosclerosis (AS), and Diabetes. Previous studies have reported that aging increases tissue susceptibility, whereas, SIRT1 regulates cellular senescence and multiple aging-related cellular processes, including SIRT1/Keap1/Nrf2/HO-1 and SIRTI/PI3K/Akt/GSK-3β mediated oxidative stress, SIRT1/NF-κB and SIRT1/NLRP3 regulated inflammatory response, SIRT1/PGC1α/eIF2α/ATF4/CHOP and SIRT1/PKD1/CREB controlled phosphorylation, SIRT1-PINK1-Parkin mediated mitochondrial damage, SIRT1/FoxO mediated autophagy, and SIRT1/FoxG1/CREB/BDNF/Trkβ-catenin mediated neuroprotective effects. In this review, we summarized the role of SIRT1 in the improvement of the attenuation effect of quercetin on aging-related diseases and the relationship between relevant signaling pathways regulated by SIRT1. Moreover, the functional regulation of quercetin in aging-related markers such as oxidative stress, inflammatory response, mitochondrial function, autophagy and apoptosis through SIRT1 was discussed. Finally, the prospects of an extracellular vesicles (EVs) as quercetin loading and delivery, and SIRT1-mediated EVs as signal carriers for treating aging-related diseases, as well as discussed the ferroptosis alleviation effects of quercetin to protect against aging-related disease via activating SIRT1. Generally, SIRT1 may serve as a promising therapeutic target in the treatment of aging-related diseases via inhibiting oxidative stress, reducing inflammatory responses, and restoring mitochondrial dysfunction.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

et al. 2022

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“…In addition, an in vitro PD model further showed that FPN1 activity in SN microglia is inhibited and iron secretion is blocked, causing pro-inflammatory transformation ( Zhang et al, 2014 ). Activation of glial cells and iron homeostasis-induced iron deposition form a “partners in crime” that alter cellular metabolic state, exacerbate oxidative distress, and induce ferroptosis on DA neurons ( Wang Z. L. et al, 2022 ).…”

Section: Emerging Links Of Ferroptosis To Neurodegenerative Diseasesmentioning

confidence: 99%

Mechanisms of Ferroptosis and Emerging Links to the Pathology of Neurodegenerative Diseases

Sun

Xia

Basnet

et al. 2022

Front. Aging Neurosci.

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Neurodegenerative diseases are a diverse class of diseases attributed to chronic progressive neuronal degeneration and synaptic loss in the brain and/or spinal cord, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis and multiple sclerosis. The pathogenesis of neurodegenerative diseases is complex and diverse, often involving mitochondrial dysfunction, neuroinflammation, and epigenetic changes. However, the pathogenesis of neurodegenerative diseases has not been fully elucidated. Recently, accumulating evidence revealed that ferroptosis, a newly discovered iron-dependent and lipid peroxidation-driven type of programmed cell death, provides another explanation for the occurrence and progression of neurodegenerative diseases. Here, we provide an overview of the process and regulation mechanisms of ferroptosis, and summarize current research progresses that support the contribution of ferroptosis to the pathogenesis of neurodegenerative diseases. A comprehensive understanding of the emerging roles of ferroptosis in neurodegenerative diseases will shed light on the development of novel therapeutic technologies and strategies for slowing down the progression of these diseases.

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“…The main toxic component of Lewy bodies is the protein a-synuclein which plays a pivotal role in PD pathogenesis. There are several key molecular pathogenic mechanisms-including genetic factors, a-synuclein aggregation, impairment of protein clearance, mitochondrial dysfunction, ferroptosis, neuroinflammation, and oxidative stress-involved in PD pathogenesis (11)(12)(13). The exact PD pathogenesis is yet to be completely elucidated owing to the multifactorial nature of the disease, leading to the lack of disease-modifying treatment strategies.…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota: A Novel Therapeutic Target for Parkinson’s Disease

Zhu

Liu

et al. 2022

Front. Immunol.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease characterized by motor dysfunction. Growing evidence has demonstrated that gut dysbiosis is involved in the occurrence, development and progression of PD. Numerous clinical trials have identified the characteristics of the changed gut microbiota profiles, and preclinical studies in PD animal models have indicated that gut dysbiosis can influence the progression and onset of PD via increasing intestinal permeability, aggravating neuroinflammation, aggregating abnormal levels of α-synuclein fibrils, increasing oxidative stress, and decreasing neurotransmitter production. The gut microbiota can be considered promising diagnostic and therapeutic targets for PD, which can be regulated by probiotics, psychobiotics, prebiotics, synbiotics, postbiotics, fecal microbiota transplantation, diet modifications, and Chinese medicine. This review summarizes the recent studies in PD-associated gut microbiota profiles and functions, the potential roles, and mechanisms of gut microbiota in PD, and gut microbiota-targeted interventions for PD. Deciphering the underlying roles and mechanisms of the PD-associated gut microbiota will help interpret the pathogenesis of PD from new perspectives and elucidate novel therapeutic strategies for PD.

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Ferroptosis in Parkinson’s disease: glia–neuron crosstalk

Cited by 149 publications

References 102 publications

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism

Mechanisms of Ferroptosis and Emerging Links to the Pathology of Neurodegenerative Diseases

Gut Microbiota: A Novel Therapeutic Target for Parkinson’s Disease

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