Reactive Oxygen Species in Metabolic and Inflammatory Signaling

Circulation Research, Journal Year: 2018, Volume and Issue: 122(6), P. 877 - 902

Published: March 15, 2018

Reactive oxygen species (ROS) are well known for their role in mediating both physiological and pathophysiological signal transduction. Enzymes subcellular compartments that typically produce ROS associated with metabolic regulation, diseases dysfunction may be influenced by changes redox balance. In this review, we summarize the current literature surrounding inflammatory focusing on transduction its relationship to disease progression. particular, examine production such as cytoplasm, mitochondria, peroxisome, endoplasmic reticulum discuss how influence processes proteasome function, autophagy, general signaling. We also highlight of regulation metabolic/inflammatory including atherosclerosis, diabetes mellitus, stroke. order develop therapies target oxidative signaling, it is vital understand balance signaling plays physiology pathophysiology, manipulation identity cellular tissue homeostasis. An increased understanding specific sources an appreciation metabolism help guide us effort treat cardiovascular diseases.

Language: Английский

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Calcium and ROS: A mutual interplay

Redox Biology, Journal Year: 2015, Volume and Issue: 6, P. 260 - 271

Published: Aug. 11, 2015

Calcium is an important second messenger involved in intra- and extracellular signaling cascades plays essential role cell life death decisions. The Ca2+ network works many different ways to regulate cellular processes that function over a wide dynamic range due the action of buffers, pumps exchangers on plasma membrane as well internal stores. pathways interact with other systems such reactive oxygen species (ROS). Although initially considered be potentially detrimental byproducts aerobic metabolism, it now clear ROS generated sub-toxic levels by intracellular act molecules various including growth death. Increasing evidence suggests mutual interplay between calcium which seems have implications for fine tuning networks. However, dysfunction either might affect system thus potentiating harmful effects contribute pathogenesis disorders.

Language: Английский

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Reperfusion injury and reactive oxygen species: The evolution of a concept

Redox Biology, Journal Year: 2015, Volume and Issue: 6, P. 524 - 551

Published: Oct. 20, 2015

Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following restoration of flow oxygenation, has been a focus basic clinical research for over 4-decades. While variety molecular mechanisms have proposed to explain this phenomenon, excess production reactive oxygen species (ROS) continues receive much attention as critical factor in genesis reperfusion injury. As consequence, considerable effort devoted identifying dominant cellular enzymatic sources ROS ischemia-reperfusion (I/R). Of potential described date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, uncoupled nitric oxide synthase gained status most likely contributors reperfusion-induced oxidative stress represent priority targets therapeutic intervention against organ dysfunction damage. Although all four are present tissues play some role emphasis given specific enriched certain tissues, such gastrointestinal tract mitochondria metabolically active heart brain. The possibility multiple contribute injury supported evidence demonstrating redox-signaling enables produced one source (e.g., Nox) activate enhance second mitochondria). This review provides synopsis implicating implications summarizes current understanding frequently invoked post-ischemic tissue.

Language: Английский

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Current Mechanistic Concepts in Ischemia and Reperfusion Injury

Cellular Physiology and Biochemistry, Journal Year: 2018, Volume and Issue: 46(4), P. 1650 - 1667

Published: Jan. 1, 2018

Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially involvement reactive oxygen species cell death pathways. The NADPH oxidase system, nitric oxide synthase xanthine system are also described. When blood supply re-established after prolonged ischemia, local inflammation ROS production increase, leading to secondary injury. Cell damage induced by may lead apoptosis, autophagy, necrosis, necroptosis. We highlight latest mechanistic insights into reperfusion-injury-induced via these different processes. interlinked signaling pathways could offer new targets approaches. Treatment approaches reviewed. believe understanding will enable development novel treatment interventions.

Language: Английский

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Ischemia/Reperfusion

Comprehensive physiology, Journal Year: 2016, Volume and Issue: unknown, P. 113 - 170

Published: Dec. 6, 2016

Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease death in westernized cultures. The extent tissue injury relates directly to blood flow reduction length ischemic period, which influence levels cellular ATP intracellular pH reduced. By impairing ATPase-dependent ion transport, ischemia mitochondrial calcium increase (calcium overload). Cell volume regulatory mechanisms also disrupted by lack ATP, can induce lysis organelle plasma membranes. Reperfusion, although required salvage oxygen-starved tissues, produces paradoxical responses that fuel production reactive oxygen species (oxygen paradox), sequestration proinflammatory immunocytes endoplasmic reticulum stress, development postischemic capillary no-reflow, amplify injury. These pathologic events culminate opening permeability transition pores a end-effector ischemia/reperfusion (I/R)-induced cell death. Emerging concepts include intestinal microbiome, fetal programming, epigenetic changes, microparticles pathogenesis I/R. overall goal this review is describe these other contribute I/R Because so many different deleterious participate I/R, it clear therapeutic approaches will be effective only when multiple processes targeted. In addition, translational significance research enhanced much wider use animal models incorporate complicating effects risk factors for cardiovascular disease. © 2017 American Physiological Society. Compr Physiol 7:113-170, 2017.

Language: Английский

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Blood flow restriction training in clinical musculoskeletal rehabilitation: a systematic review and meta-analysis

British Journal of Sports Medicine, Journal Year: 2017, Volume and Issue: 51(13), P. 1003 - 1011

Published: March 4, 2017

Background and objective

Low-load exercise training with blood flow restriction (BFR) can increase muscle strength may offer an effective clinical musculoskeletal (MSK) rehabilitation tool. The aim of this review was to systematically analyse the evidence regarding effectiveness novel modality in MSK rehabilitation.

Design

This is a systematic meta-analysis peer-reviewed literature examining BFR (Research Registry; researchregistry91).

Data sources

A search conducted across SPORTDiscus (EBSCO), PubMed Science Direct databases, including reference lists relevant papers. Two independent reviewers extracted study characteristics functional outcome measures. Study quality reporting assessed using Tool for assEssment qualiTy EXercise.

Eligibility

Search results were limited studies investigating rehabilitation, published scientific journal English.

Results

Twenty eligible, ACL reconstruction (n=3), knee osteoarthritis older adults at risk sarcopenia (n=13) patients sporadic inclusion body myositis (n=1). Analysis pooled data indicated low-load had moderate effect on increasing (Hedges’ g=0.523, 95% CI 0.263 0.784, p<0.001), but less than heavy-load g=0.674, 0.296 1.052, p<0.001).

Conclusion

Compared training, more effective, tolerable therefore potential There need development individualised approach prescription minimise patient effectiveness.

Language: Английский

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Free Radical Damage in Ischemia‐Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy

Oxidative Medicine and Cellular Longevity, Journal Year: 2018, Volume and Issue: 2018(1)

Published: Jan. 1, 2018

Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator endovascular thrombectomy are the main revascularization therapies for acute stroke. However, ischemia-reperfusion injury after therapy can result in worsening outcomes. Among all possible pathological mechanisms injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play key role process. Free radicals lead protein dysfunction, DNA damage, lipid peroxidation, resulting cell death. Additionally, strong connection inducing hemorrhagic transformation cerebral edema, which major complications therapy, mainly influencing neurological outcomes due disruption blood-brain barrier. In order get better clinical prognosis, more studies focus on pharmaceutical nonpharmaceutical neuroprotective against damage. This review discusses adjunctive combined

Language: Английский

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Abiotic stress: Interplay between ROS, hormones and MAPKs

Environmental and Experimental Botany, Journal Year: 2017, Volume and Issue: 137, P. 142 - 157

Published: Feb. 17, 2017

Language: Английский

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Diverse roles of mitochondria in ischemic stroke

Redox Biology, Journal Year: 2018, Volume and Issue: 16, P. 263 - 275

Published: March 9, 2018

Stroke is the leading cause of adult disability and mortality in most developing developed countries. The current best practices for patients with acute ischemic stroke include intravenous tissue plasminogen activator endovascular thrombectomy large-vessel occlusion to improve clinical outcomes. However, only a limited portion receive thrombolytic therapy or treatment because therapeutic time window after narrow. To address shortage management approaches, it critical identify new potential targets. mitochondrion an often overlooked target stroke. Early studies mitochondria focused on their bioenergetic role; however, these organelles are now known be important wide range cellular functions signaling events. This review aims summarize knowledge mitochondrial molecular mechanisms underlying cerebral ischemia involved reactive oxygen species generation scavenging, electron transport chain dysfunction, apoptosis, dynamics biogenesis, inflammation. A better understanding roles ischemia-related neuronal death protection may provide rationale development innovative regimens other syndromes.

Language: Английский

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Impact of Oxidative Stress on Exercising Skeletal Muscle

Biomolecules, Journal Year: 2015, Volume and Issue: 5(2), P. 356 - 377

Published: April 10, 2015

It is well established that muscle contractions during exercise lead to elevated levels of reactive oxygen species (ROS) in skeletal muscle. These highly molecules have many deleterious effects, such as a reduction force generation and increased atrophy. Since the discovery exercise-induced oxidative stress several decades ago, evidence has accumulated ROS produced also positive effects by influencing cellular processes expression antioxidants. are particularly regularly exercising prevent negative neutralizing free radicals. In addition, seem be involved adaptation phenotype. This review provides an overview evidences date on aspects include sources ROS, their role antioxidants, present ROS-dependent adaptations cells response physical exercise.

Language: Английский

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