Relationship Between Redox Status and Cell Fate in Immunity and Autoimmunity

Ortona, Elena; Maselli, Angela; Delunardo, Federica; Colasanti, Tania; Giovannetti, Antonello; Pierdominici, Marina

doi:10.1089/ars.2013.5752

Cited by 26 publications

(24 citation statements)

References 197 publications

(193 reference statements)

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“…For example, mtROS can increase mitochondrial permeability (by opening of the mitochondrial permeability transition pore) with subsequent release of (oxidized) mtDNA, which represents a damage-associated molecular pattern (DAMP) and initiates a process called “sterile inflammation” (Figure 2) [100, 200]. Other examples for the contribution of ROS to inflammation pathways are redox-dependent formation of protein complexes (e.g., p53-JNK, Nrf2-Keap1), redox regulation of mediators of inflammation (e.g., HMGB1, S100 proteins, and DAMPs), and redox modulation of transcription factors involved in inflammatory pathways (e.g., Nrf2, AP-1, NF- κ B, and HIF-1 α ) [201–203]. Additional recent evidence linking oxidative stress, inflammation, and the development of hypertension lies in the formation of isoketals, highly reactive compounds that form protein adducts that can then trigger immune cell infiltration into the vasculature and high blood pressure.…”

Section: The Molecular Triggers Of Cardiovascular Diseasementioning

confidence: 99%

Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease

Steven

Frenis

Oelze

et al. 2019

Oxidative Medicine and Cellular Longevity

503

333

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Cardiovascular disease is a leading cause of death and reduced quality of life, proven by the latest data of the Global Burden of Disease Study, and is only gaining in prevalence worldwide. Clinical trials have identified chronic inflammatory disorders as cardiovascular risks, and recent research has revealed a contribution by various inflammatory cells to vascular oxidative stress. Atherosclerosis and cardiovascular disease are closely associated with inflammation, probably due to the close interaction of inflammation with oxidative stress. Classical therapies for inflammatory disorders have demonstrated protective effects in various models of cardiovascular disease; especially established drugs with pleiotropic immunomodulatory properties have proven beneficial cardiovascular effects; normalization of oxidative stress seems to be a common feature of these therapies. The close link between inflammation and redox balance was also supported by reports on aggravated inflammatory phenotype in the absence of antioxidant defense proteins (e.g., superoxide dismutases, heme oxygenase-1, and glutathione peroxidases) or overexpression of reactive oxygen species producing enzymes (e.g., NADPH oxidases). The value of immunomodulation for the treatment of cardiovascular disease was recently supported by large-scale clinical trials demonstrating reduced cardiovascular mortality in patients with established atherosclerotic disease when treated by highly specific anti-inflammatory therapies (e.g., using monoclonal antibodies against cytokines). Modern antidiabetic cardiovascular drugs (e.g., SGLT2 inhibitors, DPP-4 inhibitors, and GLP-1 analogs) seem to share these immunomodulatory properties and display potent antioxidant effects, all of which may explain their successful lowering of cardiovascular risk.

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Section: The Molecular Triggers Of Cardiovascular Diseasementioning

confidence: 99%

Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease

Steven

Frenis

Oelze

et al. 2019

Oxidative Medicine and Cellular Longevity

503

333

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“…In fact, reactive species generated in endothelial cells, as a consequence of coronary microvascular inflammation, have been proposed to propagate the damage to cardiomyocytes through paracrine mechanisms, contributing to the maladaptive cardiac remodeling [38,46]. Notably, the association between ROS production and inflammatory processes has been extensively reported in the literature and may play a role in cardiovascular diseases [47–50].…”

Section: Reactive Oxygen and Nitrogen Species In Heart Failurementioning

confidence: 99%

Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities

Kiyuna

Albuquerque

Chen

et al. 2018

Free Radical Biology and Medicine

159

131

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Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure. In this review we discuss the most recent findings on the central role of mitochondrial dysfunction, oxidative stress and aldehydic load in heart failure, highlighting the most recent preclinical and clinical studies using mitochondria-targeted molecules and exercise training as effective tools against heart failure.

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“…More recently, the involvement of the immune system in the development of vascular dysfunction (Karbach et al , ) and the “ROS‐induced ROS concept” further contributed to the complexity of this crosstalk hypothesis but also provided new explanations on so far unanswered questions (Zorov et al , ). Of note, mitochondrial ROS were reported to activate the NLRP3 inflammasome (Zhou et al , ), promote the expression of proinflammatory cytokines in LPS‐induced sepsis (Bulua et al , ) and improve bactericidal activity (West et al , ) (for review see (Ortona et al , )). Putting together these lines of evidence with recent data on redox activation of immune cells by mitochondrial superoxide/hydrogen peroxide formation (Dikalov et al ., ; Kroller‐Schon et al , ) provides the basis for tight association between redox regulatory pathways and inflammation.…”

Section: Conclusion and Clinical Implicationsmentioning

confidence: 99%

Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function

Daiber

Lisa

Oelze

et al. 2016

British J Pharmacology

228

202

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Cardiovascular diseases are associated with and/or caused by oxidative stress. This concept has been proven by using the approach of genetic deletion of reactive species producing (pro-oxidant) enzymes as well as by the overexpression of reactive species detoxifying (antioxidant) enzymes leading to a marked reduction of reactive oxygen and nitrogen species (RONS) and in parallel to an amelioration of the severity of diseases. Likewise, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of antioxidant RONS detoxifying enzymes. Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis). Pathways and potential mechanisms leading to this crosstalk will be analysed in detail and highlighted by selected examples from the current literature including hypoxia, angiotensin II-induced hypertension, nitrate tolerance, aging and others. The general concept of redox-based activation of RONS sources via "kindling radicals" and enzyme-specific "redox switches" will be discussed providing evidence that mitochondria represent key players and amplifiers of the burden of oxidative stress. LINKED ARTICLESThis article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc Abbreviations ΔΨ m , mitochondrial membrane potential; 5-HD, 5-hydroxydecanoic acid; ADMA, asymmetric dimethylarginine; AT-II, angiotensin-II; BH 4 , tetrahydrobiopterin; cGMP, cyclic guanosine monophosphate; COX, cyclooxygenase; eNOS, endothelial nitric oxide synthase; ET-1, endothelin-1; GCH-1, GTP cyclohydrolase-1; K ATP ,, ATP-sensitive potassium channel; MAO, monoamine oxidase (isoforms A and B); MAPK, mitogen-activated protein kinases; MitoSOX, triphenylphosphonium dihydroethidium (mitochondria-targeted superoxide probe); MitoQ, triphenylphosphonium quinone (mitochondria-targeted antioxidant); MnSOD, manganese superoxide dismutase; mPTP, mitochondrial permeability transition pore; mtK ATP ,, mitochondrial K ATP ; mtROS, mitochondrial reactive oxygen species; nNOS, neuronal nitric oxide synthase; Nox, NADPH oxidase catalytic subunit (isoforms 1, 2 and 4); PGIS, prostacyclin; PKC, protein kinase C; RNS, reactive nitrogen species (accounts in the present review mostly for peroxynitrite and nitrogen dioxide); ROS, reactive oxygen species (accounts in the present review mostly for superoxide and hydrogen peroxide); sGC, soluble guanylyl cyclase; SOD, superoxide dismutase; Src (or cSrc), tyrosine kinase; XDH, xanthine dehydrogenase; XO, xanthine oxidase...

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Relationship Between Redox Status and Cell Fate in Immunity and Autoimmunity

Abstract: Deciphering the intricate relationships between oxidative stress and both apoptosis and autophagy in the context of autoimmunity could be critical in elucidating key pathogenic mechanisms and could lead to novel interventions for the clinical management of autoimmune diseases.

Cited by 26 publications

References 197 publications

Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease

Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease

Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities

Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function

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