Elevated Glucose Levels Favor SARS-CoV-2 Infection and Monocyte Response through a HIF-1α/Glycolysis-Dependent Axis

Cell Metabolism, Journal Year: 2020, Volume and Issue: 32(3), P. 437 - 446.e5

Published: July 17, 2020

Language: Английский

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Mitochondrial dynamics in health and disease: mechanisms and potential targets

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: Sept. 6, 2023

Abstract Mitochondria are organelles that able to adjust and respond different stressors metabolic needs within a cell, showcasing their plasticity dynamic nature. These abilities allow them effectively coordinate various cellular functions. Mitochondrial dynamics refers the changing process of fission, fusion, mitophagy transport, which is crucial for optimal function in signal transduction metabolism. An imbalance mitochondrial can disrupt function, leading abnormal fate, range diseases, including neurodegenerative disorders, cardiovascular diseases cancers. Herein, we review mechanism dynamics, its impacts on function. We also delve into changes occur during health disease, offer novel perspectives how target modulation dynamics.

Language: Английский

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Redox regulation of the immune response

Cellular and Molecular Immunology, Journal Year: 2022, Volume and Issue: 19(10), P. 1079 - 1101

Published: Sept. 2, 2022

Abstract The immune-inflammatory response is associated with increased nitro-oxidative stress. aim of this mechanistic review to examine: (a) the role redox-sensitive transcription factors and enzymes, ROS/RNS production, activity cellular antioxidants in activation performance macrophages, dendritic cells, neutrophils, T-cells, B-cells, natural killer cells; (b) involvement high-density lipoprotein (HDL), apolipoprotein A1 (ApoA1), paraoxonase-1 (PON1), oxidized phospholipids regulating immune response; (c) detrimental effects hypernitrosylation chronic stress on response. redox changes during responses are orchestrated by actions nuclear factor-κB, HIF1α, target rapamycin, phosphatidylinositol 3-kinase/protein kinase B signaling pathway, mitogen-activated protein kinases, 5' AMP-activated kinase, peroxisome proliferator-activated receptor. survival individual cells under control depends intracellular extracellular levels ROS/RNS. They heavily influenced including glutathione thioredoxin systems, factor erythroid 2-related 2, HDL/ApoA1/PON1 complex. Chronic inhibit those antioxidant tricarboxylic acid cycle, mitochondrial functions, metabolism cells. In conclusion, redox-associated mechanisms modulate metabolic reprogramming macrophage T helper cell polarization, phagocytosis, production pro- versus anti-inflammatory cytokines, training tolerance, chemotaxis, pathogen sensing, antiviral antibacterial effects, Toll-like receptor activity, endotoxin tolerance.

Language: Английский

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Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome

Proceedings of the National Academy of Sciences, Journal Year: 2021, Volume and Issue: 118(34)

Published: Aug. 16, 2021

Although most patients recover from acute COVID-19, some experience postacute sequelae of severe respiratory syndrome coronavirus 2 infection (PASC). One subgroup PASC is a called "long COVID-19," reminiscent myalgic encephalomyelitis/chronic fatigue (ME/CFS). ME/CFS debilitating condition, often triggered by viral and bacterial infections, leading to years-long symptoms including profound fatigue, postexertional malaise, unrefreshing sleep, cognitive deficits, orthostatic intolerance. Some are skeptical that either or long COVID-19 involves underlying biological abnormalities. However, in this review, we summarize the evidence people with have abnormalities redox imbalance, systemic inflammation neuroinflammation, an impaired ability generate adenosine triphosphate, general hypometabolic state. These phenomena not yet been well studied each them has reported other diseases as well, particularly neurological diseases. We also examine bidirectional relationship between inflammation, energy metabolic speculate what may be causing these Thus, understanding molecular underpinnings both lead development novel therapeutics.

Language: Английский

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Chronic Inflammation in Chronic Kidney Disease Progression: Role of Nrf2

Kidney International Reports, Journal Year: 2021, Volume and Issue: 6(7), P. 1775 - 1787

Published: May 4, 2021

Language: Английский

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Shaping Neuronal Fate: Functional Heterogeneity of Direct Microglia-Neuron Interactions

Neuron, Journal Year: 2020, Volume and Issue: 109(2), P. 222 - 240

Published: Dec. 2, 2020

Language: Английский

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Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(20), P. 11047 - 11047

Published: Oct. 13, 2021

Until recently, radiation effects have been considered to be mainly due nuclear DNA damage and their management by repair mechanisms. However, molecular biology studies reveal that the outcomes of exposures ionizing (IR) highly depend on activation regulation through other components organelles determine cell survival proliferation capacities. As typical epigenetic-regulated central power stations cells, mitochondria play an important pivotal role in those responses. They direct cellular metabolism, energy supply homeostasis as well radiation-induced signaling, death, immunological This review is focused how energy, dose quality IR affect mitochondria-dependent epigenetic functional control at tissue level. Low-dose appear associated with non-targeted involved genomic instability adaptive responses, whereas high-dose (>1 Gy) concern therapeutic long-term involving mitochondria-mediated innate immune Both quality. For example, increased efficacy high linear transfer particle radiotherapy, e.g., C-ion relies reduction anastasis, enhanced apoptosis immunogenic (antitumor)

Language: Английский

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The Impact of HIV- and ART-Induced Mitochondrial Dysfunction in Cellular Senescence and Aging

Cells, Journal Year: 2021, Volume and Issue: 10(1), P. 174 - 174

Published: Jan. 16, 2021

According to the WHO, 38 million individuals were living with human immunodeficiency virus (HIV), 25.4 of which using antiretroviral therapy (ART) at end 2019. Despite ART-mediated suppression viral replication, ART is not a cure and associated persistence, residual inflammation, metabolic disturbances. Indeed, due presence reservoirs, lifelong required control viremia prevent disease progression into acquired immune deficiency syndrome (AIDS). Successful treatment allows people HIV (PLHIV) achieve similar life expectancy uninfected individuals. However, recent studies have illustrated increased comorbidities, such as accelerated, premature aging, in ART-controlled PLHIV compared Studies suggest that both HIV-infection ART-treatment lead mitochondrial dysfunction, ultimately resulting cellular exhaustion, senescence, apoptosis. Since mitochondria are essential organelles for energy homeostasis metabolism, their compromise leads decreased oxidative phosphorylation (OXPHOS), ATP synthesis, gluconeogenesis, beta-oxidation, abnormal cell homeostasis, stress, depolarization membrane potential, upregulation DNA mutations The progressive damage induced by likely contributes accelerated dysfunction PLHIV. This review discusses connections between HIV- ART-induced toxicities, providing new insights how current directly impact functions contribute senescence aging Identifying this nexus potential mechanisms may be beneficial developing improved therapeutics treating

Language: Английский

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The Impact of Fine Particulate Matter 2.5 on the Cardiovascular System: A Review of the Invisible Killer

Nanomaterials, Journal Year: 2022, Volume and Issue: 12(15), P. 2656 - 2656

Published: Aug. 2, 2022

Air pollution exerts several deleterious effects on the cardiovascular system, with disease (CVD) accounting for 80% of all premature deaths caused by air pollution. Short-term exposure to particulate matter 2.5 (PM2.5) leads acute CVD-associated and nonfatal events, whereas long-term increases risk death reduces longevity. Here, we summarize published data illustrating how PM2.5 may impact system provide information mechanisms which it contribute CVDs. We an overview PM2.5, its associated health risks, global statistics, mechanistic underpinnings related mitochondria, hazardous biological effects. elaborate association between CVD development examine preventive measures future strategies combating PM2.5-related adverse The insights gained can critical guidelines preventing pollution-related CVDs through governmental, societal, personal measures, thereby benefitting humanity slowing climate change.

Language: Английский

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TREM-1 governs NLRP3 inflammasome activation of macrophages by firing up glycolysis in acute lung injury

International Journal of Biological Sciences, Journal Year: 2022, Volume and Issue: 19(1), P. 242 - 257

Published: Nov. 23, 2022

The triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory immune potentiating acute lung injury (ALI).However, the mechanism of TREM-1-triggered inflammation response remains poorly understood.Here, we showed that TREM-1 blocking attenuated NOD-, LRRand pyrin domain-containing 3 (NLRP3) inflammasome activation and glycolysis in LPS-induced ALI mice.Then, observed enhanced glucose consumption, induced glycolysis, inhibited oxidative phosphorylation macrophages.Specifically, inhibition with 2-deoxyglucose diminished NLRP3 macrophages triggered by TREM-1.Hypoxia-inducible factor-1α (HIF-1α) critical transcriptional regulator glycolysis.We further found facilitated HIF-1α accumulation translocation to nucleus via phosphoinositide 3-kinase (PI3K)/AKT/mammalian target rapamycin (mTOR) pathway.Inhibiting mTOR or also suppressed TREM-1-induced metabolic reprogramming NLRP3/caspase-1 activation.Overall, mTOR/HIF-1α/glycolysis pathway novel underlying TREM-1-governed activation.Therapeutic targeting TREM-1-activated could be beneficial for treating preventing inflammatory diseases, such as ALI.

Language: Английский

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