scholarly journals MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

2020 ◽  
Vol 21 (12) ◽  
pp. 4370
Author(s):  
Montserrat Climent ◽  
Giacomo Viggiani ◽  
Ya-Wen Chen ◽  
Gerald Coulis ◽  
Alessandra Castaldi
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Redox Balance ◽  
Chronic Obstructive ◽  
Transcriptional Level ◽  
Control Mechanisms ◽  
Redox Equilibrium ◽  
Obstructive Pulmonary Disease

Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

scholarly journals Bilirubin acts as a multipotent guardian of cardiovascular integrity: more than just a radical idea

2018 ◽  
Vol 315 (3) ◽  
pp. H429-H447 ◽  
Author(s):  
Andrew C. Bulmer ◽  
Bhavisha Bakrania ◽  
Eugene F. Du Toit ◽  
Ai-Ching Boon ◽  
Paul J. Clark ◽  
...  
Keyword(s):  
Clinical Medicine ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Chronic Obstructive ◽  
Protective Properties ◽  
Physiological Importance ◽  
Bilirubin Excretion ◽  
Chronic Obstructive Pulmonary Diseases ◽  
Atherosclerotic Process

Bilirubin, a potentially toxic catabolite of heme and indicator of hepatobiliary insufficiency, exhibits potent cardiac and vascular protective properties. Individuals with Gilbert’s syndrome (GS) may experience hyperbilirubinemia in response to stressors including reduced hepatic bilirubin excretion/increased red blood cell breakdown, with individuals usually informed by their clinician that their condition is of little consequence. However, GS appears to protect from all-cause mortality, with progressively elevated total bilirubin associated with protection from ischemic heart and chronic obstructive pulmonary diseases. Bilirubin may protect against these diseases and associated mortality by reducing circulating cholesterol, oxidative lipid/protein modifications, and blood pressure. In addition, bilirubin inhibits platelet activation and protects the heart from ischemia-reperfusion injury. These effects attenuate multiple stages of the atherosclerotic process in addition to protecting the heart during resultant ischemic stress, likely underpinning the profound reduction in cardiovascular mortality in hyperbilirubinemic GS. This review outlines our current knowledge of and uses for bilirubin in clinical medicine and summarizes recent progress in revealing the physiological importance of this poorly understood molecule. We believe that this review will be of significant interest to clinicians, medical researchers, and individuals who have GS.

scholarly journals Heat Shock Proteins in Oxidative Stress and Ischemia/Reperfusion Injury and Benefits from Physical Exercises: A Review to the Current Knowledge

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jakub Szyller ◽  
Iwona Bil-Lula
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Physical Exercises ◽  
Shock Proteins

Heat shock proteins (HSPs) are molecular chaperones produced in response to oxidative stress (OS). These proteins are involved in the folding of newly synthesized proteins and refolding of damaged or misfolded proteins. Recent studies have been focused on the regulatory role of HSPs in OS and ischemia/reperfusion injury (I/R) where reactive oxygen species (ROS) play a major role. ROS perform many functions, including cell signaling. Unfortunately, they are also the cause of pathological processes leading to various diseases. Biological pathways such as p38 MAPK, HSP70 and Akt/GSK-3β/eNOS, HSP70, JAK2/STAT3 or PI3K/Akt/HSP70, and HSF1/Nrf2-Keap1 are considered in the relationship between HSP and OS. New pathophysiological mechanisms involving ROS are being discovered and described the protein network of HSP interactions. Understanding of the mechanisms involved, e.g., in I/R, is important to the development of treatment methods. HSPs are multifunctional proteins because they closely interact with the antioxidant and the nitric oxide generation systems, such as HSP70/HSP90/NOS. A deficiency or excess of antioxidants modulates the activation of HSF and subsequent HSP biosynthesis. It is well known that HSPs are involved in the regulation of several redox processes and play an important role in protein-protein interactions. The latest research focuses on determining the role of HSPs in OS, their antioxidant activity, and the possibility of using HSPs in the treatment of I/R consequences. Physical exercises are important in patients with cardiovascular diseases, as they affect the expression of HSPs and the development of OS.

scholarly journals Oxidative Stress as a Mediator of Cardiovascular Disease

2009 ◽  
Vol 2 (5) ◽  
pp. 259-269 ◽  
Author(s):  
Maqsood M. Elahi ◽  
Yu Xiang Kong ◽  
Bashir M. Matata
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox Balance ◽  
Reactive Oxidant Species ◽  
Reactive Oxidant

During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species originating from a variety of sources such as nitric oxide (NO) synthase (NOS), xanthine oxidases (XO), the cyclooxygenases, nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase isoforms and metal-catalyzed reactions. In addition, we present a treatise on the physiological defences such as specialized enzymes and antioxidants that maintain reduction-oxidation (redox) balance. We have also given an account of how enzymes and antioxidants can be exhausted by the excessive production of reactive oxidant species (ROS) resulting in oxidative stress/nitrosative stress, a process that is an important mediator of cell damage. Important aspects of redox imbalance that triggers the activity of a number of signaling pathways including transcription factors activity, a process that is ubiquitous in cardiovascular disease related to ischemia/reperfusion injury have also been presented.

scholarly journals Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

2020 ◽  
Vol 21 (23) ◽  
pp. 9317
Author(s):  
Javier Checa ◽  
Josep M. Aran
Keyword(s):  
Oxidative Stress ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Structural Cell ◽  
Environmental Threats ◽  
Chronic Lung Diseases ◽  
Cell Components ◽  
Respiratory Pathology

As aerobic organisms, we are continuously and throughout our lifetime subjected to an oxidizing atmosphere and, most often, to environmental threats. The lung is the internal organ most highly exposed to this milieu. Therefore, it has evolved to confront both oxidative stress induced by reactive oxygen species (ROS) and a variety of pollutants, pathogens, and allergens that promote inflammation and can harm the airways to different degrees. Indeed, an excess of ROS, generated intrinsically or from external sources, can imprint direct damage to key structural cell components (nucleic acids, sugars, lipids, and proteins) and indirectly perturb ROS-mediated signaling in lung epithelia, impairing its homeostasis. These early events complemented with efficient recognition of pathogen- or damage-associated recognition patterns by the airway resident cells alert the immune system, which mounts an inflammatory response to remove the hazards, including collateral dead cells and cellular debris, in an attempt to return to homeostatic conditions. Thus, any major or chronic dysregulation of the redox balance, the air–liquid interface, or defects in epithelial proteins impairing mucociliary clearance or other defense systems may lead to airway damage. Here, we review our understanding of the key role of oxidative stress and inflammation in respiratory pathology, and extensively report current and future trends in antioxidant and anti-inflammatory treatments focusing on the following major acute and chronic lung diseases: acute lung injury/respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis.

The role of oxidative stress in lung injury induced by cigarette smoke

Biologia ◽  
2006 ◽  
Vol 61 (6) ◽  
Author(s):  
Zuzana Kluchová ◽  
Ružena Tkáčová
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoking ◽  
Lung Injury ◽  
Cigarette Smoke ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Systemic Circulation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Markers Of Oxidative Stress

AbstractOxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities — the state of “oxidative stress” — is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

scholarly journals Nrf2 as a Key Player of Redox Regulation in Cardiovascular Diseases

2016 ◽  
pp. S1-S10 ◽  
Author(s):  
M. BARANČÍK ◽  
L. GREŠOVÁ ◽  
M. BARTEKOVÁ ◽  
I. DOVINOVÁ
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Redox Regulation ◽  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Redox Homeostasis ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

The oxidative stress plays an important role in the development of cardiovascular diseases (CVD). In CVD progression an aberrant redox regulation was observed. In this regulation levels of reactive oxygen species (ROS) play an important role in cellular signaling, where Nrf2 is the key regulator of redox homeostasis. Keap1-Nrf2-ARE system regulates a great set of detoxificant and antioxidant enzymes in cells after ROS and electrophiles exposure. In this review we focus on radical-generating systems in cardiovascular system as well as on Nrf2 as a target against oxidative stress and a key player of redox regulation in cardiovascular diseases. We also summarize the current knowledge about the role of Nrf2 in pathophysiology of several CVD (hypertension, cardiac hypertrophy, cardiomyopathies) as well as in cardioprotection against myocardial ischemia/ reperfusion injury.

scholarly journals Recent Progress of Ferroptosis in Lung Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Shangjiang Yu ◽  
Jinqiu Jia ◽  
Jinyu Zheng ◽  
Yiyang Zhou ◽  
Danyun Jia ◽  
...  
Keyword(s):  
Lung Diseases ◽  
Acid Metabolism ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Lipid Peroxides ◽  
Research Progress ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
New Ideas ◽  
Pulmonary Ischemia

Ferroptosis is a new form of programmed cell death due to iron-dependent excess accumulation of lipid peroxides and differs from other programmed cell deaths in morphological and biochemical characteristics. The process of ferroptosis is precisely regulated by iron metabolism, lipid metabolism, amino acid metabolism, and numerous signaling pathways, and plays a complex role in many pathophysiological processes. Recent studies have found that ferroptosis is closely associated with the development and progression of many lung diseases, including acute lung injury, pulmonary ischemia-reperfusion injury, lung cancer, chronic obstructive pulmonary disease, and pulmonary fibrosis. Here, we present a review of the main regulatory mechanisms of ferroptosis and its research progress in the pathogenesis and treatment of lung diseases, with the aim of providing new ideas for basic and clinical research of lung-related diseases.

scholarly journals Carnitine Palmitoyltransferase System: A New Target for Anti-Inflammatory and Anticancer Therapy?

2021 ◽  
Vol 12 ◽  
Author(s):  
Muyun Wang ◽  
Kun Wang ◽  
Ximing Liao ◽  
Haiyang Hu ◽  
Liangzhi Chen ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Current Knowledge ◽  
Ischemia Reperfusion ◽  
Carnitine Palmitoyltransferase ◽  
Acid Oxidation ◽  
Chronic Obstructive ◽  
Hepatic Ischemia ◽  
Kidney Fibrosis ◽  
Nonalcoholic Fatty Liver ◽  
Anti Inflammatory

Lipid metabolism involves multiple biological processes. As one of the most important lipid metabolic pathways, fatty acid oxidation (FAO) and its key rate-limiting enzyme, the carnitine palmitoyltransferase (CPT) system, regulate host immune responses and thus are of great clinical significance. The effect of the CPT system on different tissues or organs is complex: the deficiency or over-activation of CPT disrupts the immune homeostasis by causing energy metabolism disorder and inflammatory oxidative damage and therefore contributes to the development of various acute and chronic inflammatory disorders and cancer. Accordingly, agonists or antagonists targeting the CPT system may become novel approaches for the treatment of diseases. In this review, we first briefly describe the structure, distribution, and physiological action of the CPT system. We then summarize the pathophysiological role of the CPT system in chronic obstructive pulmonary disease, bronchial asthma, acute lung injury, chronic granulomatous disease, nonalcoholic fatty liver disease, hepatic ischemia–reperfusion injury, kidney fibrosis, acute kidney injury, cardiovascular disorders, and cancer. We are also concerned with the current knowledge in either preclinical or clinical studies of various CPT activators/inhibitors for the management of diseases. These compounds range from traditional Chinese medicines to novel nanodevices. Although great efforts have been made in studying the different kinds of CPT agonists/antagonists, only a few pharmaceuticals have been applied for clinical uses. Nevertheless, research on CPT activation or inhibition highlights the pharmacological modulation of CPT-dependent FAO, especially on different CPT isoforms, as a promising anti-inflammatory/antitumor therapeutic strategy for numerous disorders.

scholarly journals COMBORIDITY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND CARDIOVASCULAR DISEASES: GENERAL FACTORS, PATHOPHYSIOLOGICAL MECHANISMS AND CLINICAL SIGNIFICANCE

2020 ◽  
Author(s):  
Aleksey Mikhailovich Chaulin ◽  
Julia Vladimirovna Grigoryeva ◽  
Dmitriy Viktorovich Duplyakov
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cardiovascular Diseases ◽  
Pulmonary Disease ◽  
Sedentary Lifestyle ◽  
Current Knowledge ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
High Prevalence ◽  
Common Risk Factors

Currently, the comorbidity (combination) of chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVD) is an relevant problem for health care. This is due to the high prevalence and continued growth of these pathologies. CVD and COPD have common risk factors and mechanisms underlying their development and progression: smoking, inflammation, sedentary lifestyle, aging, oxidative stress, air pollution, and hypoxia. In this review, we summarize current knowledge relating to the prevalence and frequency of cardiovascular diseases in people with COPD and the mechanisms that underlie their coexistence. The implications for clinical practice, in particular the main problems of diagnosis and treatment of COPD/CVD comorbidity, are also discussed.

scholarly journals Novel drug delivery systems targeting oxidative stress in chronic obstructive pulmonary disease: a review

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
You Xu ◽  
Hongmei Liu ◽  
Lei Song
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Drug Delivery ◽  
Pulmonary Disease ◽  
Drug Delivery Systems ◽  
Current Knowledge ◽  
Delivery Systems ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Novel Drug

Abstract Oxidative stress is significantly involved in the pathogenesis and progression of chronic obstructive pulmonary disease (COPD). Combining antioxidant drugs or nutrients results in a noteworthy therapeutic value in animal models of COPD. However, the benefits have not been reproduced in clinical applications, this may be attributed to the limited absorption, concentration, and half-life of exogenous antioxidants. Therefore, novel drug delivery systems to combat oxidative stress in COPD are needed. This review presents a brief insight into the current knowledge on the role of oxidative stress and highlights the recent trends in novel drug delivery carriers that could aid in combating oxidative stress in COPD. The introduction of nanotechnology has enabled researchers to overcome several problems and improve the pharmacokinetics and bioavailability of drugs. Large porous microparticles, and porous nanoparticle-encapsulated microparticles are the most promising carriers for achieving effective pulmonary deposition of inhaled medication and obtaining controlled drug release. However, translating drug delivery systems for administration in pulmonary clinical settings is still in its initial phases.

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