Peroxisomal Stress Response and Inter-Organelle Communication in Cellular Homeostasis and Aging

Kim, Jinoh; Bai, Hua

doi:10.3390/antiox11020192

Cited by 23 publications

(21 citation statements)

References 203 publications

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“…Peroxisomes crosstalk with the nucleus, mitochondria, endoplasmic reticulum (ER) and lysosomes, and these inter-organelle communications are key to maintain peroxisome function. Of note, peroxisomal dysfunction has been described in disease and during ageing and is associated with many cellular alterations, highlighting its important roles in redox homeostasis [30].…”

Section: Major Ros Sourcesmentioning

confidence: 99%

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

2023

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Reactive oxygen species (ROS) have been described to induce a broad range of redox-dependent signaling reactions in physiological conditions. Nevertheless, an excessive accumulation of ROS leads to oxidative stress, which was traditionally considered as detrimental for cells and organisms, due to the oxidative damage they cause to biomolecules. During ageing, elevated ROS levels result in the accumulation of damaged proteins, which may exhibit altered enzymatic function or physical properties (e.g., aggregation propensity). Emerging evidence also highlights the relationship between oxidative stress and age-related pathologies, such as protein misfolding-based neurodegenerative diseases (e.g., Parkinson’s (PD), Alzheimer’s (AD) and Huntington’s (HD) diseases). In this review we aim to introduce the role of oxidative stress in physiology and pathology and then focus on the state-of-the-art techniques available to detect and quantify ROS and oxidized proteins in live cells and in vivo, providing a guide to those aiming to characterize the role of oxidative stress in ageing and neurodegenerative diseases. Lastly, we discuss recently published data on the role of oxidative stress in neurological disorders.

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Section: Major Ros Sourcesmentioning

confidence: 99%

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

2023

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“…On the other hand, peroxisome (PO) has drawn increasing research interest in senescence. PO activity declines with age, and its dysfunction is associated with age-related diseases (neurodegeneration) and metabolic diseases like CVDs and obesity (Kim & Bai, 2022;Zalckvar & Schuldiner, 2022).…”

Section: Cellular Organelles and Vascular Agingmentioning

confidence: 99%

Membrane contact sites orchestrate cholesterol homeostasis that is central to vascular aging

Pang

Jin

et al. 2023

WIREs Mechanisms of Disease

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Chronological age causes structural and functional vascular deterioration and is a well‐established risk factor for the development of cardiovascular diseases, leading to more than 40% of all deaths in the elderly. The etiology of vascular aging is complex; a significant impact arises from impaired cholesterol homeostasis. Cholesterol level is balanced through synthesis, uptake, transport, and esterification, the processes executed by multiple organelles. Moreover, organelles responsible for cholesterol homeostasis are spatially and functionally coordinated instead of isolated by forming the membrane contact sites. Membrane contact, mediated by specific protein–protein interaction, pulls opposing organelles together and creates the hybrid place for cholesterol transfer and further signaling. The membrane contact‐dependent cholesterol transfer, together with the vesicular transport, maintains cholesterol homeostasis and has intimate implications in a growing list of diseases, including vascular aging‐related diseases. Here, we summarized the latest advances regarding cholesterol homeostasis by highlighting the membrane contact‐based regulatory mechanism. We also describe the downstream signaling under cholesterol homeostasis perturbations, prominently in cholesterol‐rich conditions, stimulating age‐dependent organelle dysfunction and vascular aging. Finally, we discuss potential cholesterol‐targeting strategies for therapists regarding vascular aging‐related diseases.This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology

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“…Peroxisomal fatty acid oxidation leads to high levels of H 2 O 2 generation [ 265 ]. Peroxisomal dysfunction, in part due to oxidative damage by ROS/RNS, may be responsible for the decreased levels of plasmalogens that occur in aged and diseased tissues [ 266 ]. Plasmalogen levels can be increased by taking plasmalogen precursors as supplements [ 261 ].…”

Section: Dopaminergic Neurons Are Vulnerable To Dysfunctional Mqcmentioning

confidence: 99%

NADPH and Mitochondrial Quality Control as Targets for a Circadian-Based Fasting and Exercise Therapy for the Treatment of Parkinson’s Disease

Curtis

Seeds²,

Mattson

et al. 2022

Cells

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Dysfunctional mitochondrial quality control (MQC) is implicated in the pathogenesis of Parkinson’s disease (PD). The improper selection of mitochondria for mitophagy increases reactive oxygen species (ROS) levels and lowers ATP levels. The downstream effects include oxidative damage, failure to maintain proteostasis and ion gradients, and decreased NAD+ and NADPH levels, resulting in insufficient energy metabolism and neurotransmitter synthesis. A ketosis-based metabolic therapy that increases the levels of (R)-3-hydroxybutyrate (BHB) may reverse the dysfunctional MQC by partially replacing glucose as an energy source, by stimulating mitophagy, and by decreasing inflammation. Fasting can potentially raise cytoplasmic NADPH levels by increasing the mitochondrial export and cytoplasmic metabolism of ketone body-derived citrate that increases flux through isocitrate dehydrogenase 1 (IDH1). NADPH is an essential cofactor for nitric oxide synthase, and the nitric oxide synthesized can diffuse into the mitochondrial matrix and react with electron transport chain-synthesized superoxide to form peroxynitrite. Excessive superoxide and peroxynitrite production can cause the opening of the mitochondrial permeability transition pore (mPTP) to depolarize the mitochondria and activate PINK1-dependent mitophagy. Both fasting and exercise increase ketogenesis and increase the cellular NAD+/NADH ratio, both of which are beneficial for neuronal metabolism. In addition, both fasting and exercise engage the adaptive cellular stress response signaling pathways that protect neurons against the oxidative and proteotoxic stress implicated in PD. Here, we discuss how intermittent fasting from the evening meal through to the next-day lunch together with morning exercise, when circadian NAD+/NADH is most oxidized, circadian NADP+/NADPH is most reduced, and circadian mitophagy gene expression is high, may slow the progression of PD.

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Peroxisomal Stress Response and Inter-Organelle Communication in Cellular Homeostasis and Aging

Cited by 23 publications

References 203 publications

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

Membrane contact sites orchestrate cholesterol homeostasis that is central to vascular aging

NADPH and Mitochondrial Quality Control as Targets for a Circadian-Based Fasting and Exercise Therapy for the Treatment of Parkinson’s Disease

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