Autophagy and Autophagy-Related Diseases: A Review

Ichimiya, Tadashi; Yamakawa, Tsukasa; Hirano, Takehiro; Yokoyama, Yoshihiro; Hayashi, Yoshihiko; Hirayama, Daisuke; Wagatsuma, Kohei; Itoi, Takao; Nakase, Hiroshi

doi:10.3390/ijms21238974

Cited by 173 publications

(155 citation statements)

References 156 publications

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“…Cellular stress can be associated with an imbalance of these processes, and accumulation of damaged mitochondria can drive cellular dysfunction and/or immune cell activation. Disruptions to these pathways have been linked to a wide range of diseases, including cancers and several neurodegenerative diseases ( 21 , 22 ).…”

Section: Mitochondrial Dynamicsmentioning

confidence: 99%

Mitochondria as Key Players in the Pathogenesis and Treatment of Rheumatoid Arthritis

et al. 2021

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Mitochondria are major energy-producing organelles that have central roles in cellular metabolism. They also act as important signalling hubs, and their dynamic regulation in response to stress signals helps to dictate the stress response of the cell. Rheumatoid arthritis is an inflammatory and autoimmune disease with high prevalence and complex aetiology. Mitochondrial activity affects differentiation, activation and survival of immune and non-immune cells that contribute to the pathogenesis of this disease. This review outlines what is known about the role of mitochondria in rheumatoid arthritis pathogenesis, and how current and future therapeutic strategies can function through modulation of mitochondrial activity. We also highlight areas of this topic that warrant further study. As producers of energy and of metabolites such as succinate and citrate, mitochondria help to shape the inflammatory phenotype of leukocytes during disease. Mitochondrial components can directly stimulate immune receptors by acting as damage-associated molecular patterns, which could represent an initiating factor for the development of sterile inflammation. Mitochondria are also an important source of intracellular reactive oxygen species, and facilitate the activation of the NLRP3 inflammasome, which produces cytokines linked to disease symptoms in rheumatoid arthritis. The fact that mitochondria contain their own genetic material renders them susceptible to mutation, which can propagate their dysfunction and immunostimulatory potential. Several drugs currently used for the treatment of rheumatoid arthritis regulate mitochondrial function either directly or indirectly. These actions contribute to their immunomodulatory functions, but can also lead to adverse effects. Metabolic and mitochondrial pathways are attractive targets for future anti-rheumatic drugs, however many questions still remain about the precise role of mitochondrial activity in different cell types in rheumatoid arthritis.

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Section: Mitochondrial Dynamicsmentioning

confidence: 99%

Mitochondria as Key Players in the Pathogenesis and Treatment of Rheumatoid Arthritis

et al. 2021

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“…Authors performed RNA-seq in exosomes purified from platelets activated with LPS or not finding that these two miRNAs were over-expressed in exosomes derived from LPS-treated platelets. Interestingly, these miRNAs potentially regulate phosphatidylinositol 3-kinase PI3K/Akt/mTOR pathway that is actively involved in autophagy [ 78 ] that is related with NET formation [ 79 , 80 ]. Incubation of differentiated HL-60 cells with miR-378a-3p and miR-15b-5p mimics showed that they increased NET formation directly regulating the expression of phosphoinositide-dependent kinase-1 (PDK1), an Akt activator.…”

Section: Regulation Of Netosis By Mirnasmentioning

confidence: 99%

MicroRNAs as New Regulators of Neutrophil Extracellular Trap Formation

Águila

Reyes-García

Fernández-Pérez

et al. 2021

IJMS

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Neutrophil extracellular traps (NETs) are formed after neutrophils expelled their chromatin content in order to primarily capture and eliminate pathogens. However, given their characteristics due in part to DNA and different granular proteins, NETs may induce a procoagulant response linking inflammation and thrombosis. Unraveling NET formation molecular mechanisms as well as the intracellular elements that regulate them is relevant not only for basic knowledge but also to design diagnostic and therapeutic tools that may prevent their deleterious effects observed in several inflammatory pathologies (e.g., cardiovascular and autoimmune diseases, cancer). Among the potential elements involved in NET formation, several studies have investigated the role of microRNAs (miRNAs) as important regulators of this process. miRNAs are small non-coding RNAs that have been involved in the control of almost all physiological processes in animals and plants and that are associated with the development of several pathologies. In this review, we give an overview of the actual knowledge on NETs and their implication in pathology with a special focus in cardiovascular diseases. We also give a brief overview on miRNA biology to later focus on the different miRNAs implicated in NET formation and the perspectives opened by the presented data.

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“…Among them, LC3, a ubiquitin-like protein, promotes autophagosome formation (Fujita et al, 2008;Pyo et al, 2012). It regulates the elongation and closure of the autophagic membrane by binding with phosphatidylethanolamine (Ichimiya et al, 2020). Autophagy is affected by many factors, such as endoplasmic reticulum stress (ERS), immune or inflammatory stimulation, nutritional deficiency, Ca 2+ concentration and accumulation of organelle damage (Tooze and Yoshimori, 2010;Mizushima et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

The Role of the Effects of Autophagy on NLRP3 Inflammasome in Inflammatory Nervous System Diseases

Zhao

Wang

et al. 2021

Front. Cell Dev. Biol.

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Autophagy is a stable self-sustaining process in eukaryotic cells. In this process, pathogens, abnormal proteins, and organelles are encapsulated by a bilayer membrane to form autophagosomes, which are then transferred to lysosomes for degradation. Autophagy is involved in many physiological and pathological processes. Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, containing NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and pro-caspase-1, can activate caspase-1 to induce pyroptosis and lead to the maturation and secretion of interleukin-1 β (IL-1 β) and IL-18. NLRP3 inflammasome is related to many diseases. In recent years, autophagy has been reported to play a vital role by regulating the NLRP3 inflammasome in inflammatory nervous system diseases. However, the related mechanisms are not completely clarified. In this review, we sum up recent research about the role of the effects of autophagy on NLRP3 inflammasome in Alzheimer’s disease, chronic cerebral hypoperfusion, Parkinson’s disease, depression, cerebral ischemia/reperfusion injury, early brain injury after subarachnoid hemorrhage, and experimental autoimmune encephalomyelitis and analyzed the related mechanism to provide theoretical reference for the future research of inflammatory neurological diseases.

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Autophagy and Autophagy-Related Diseases: A Review

Cited by 173 publications

References 156 publications

Mitochondria as Key Players in the Pathogenesis and Treatment of Rheumatoid Arthritis

Mitochondria as Key Players in the Pathogenesis and Treatment of Rheumatoid Arthritis

MicroRNAs as New Regulators of Neutrophil Extracellular Trap Formation

The Role of the Effects of Autophagy on NLRP3 Inflammasome in Inflammatory Nervous System Diseases

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