Interleukin-6 related signaling pathways as the intersection between chronic diseases and sepsis

Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)

Published: Jan. 31, 2025

Sepsis is associated with immune dysregulated and organ dysfunction due to severe infection. Clinicians aim restore function, rather than prevent diseases that are prone sepsis, resulting in high mortality a heavy public health burden. Some chronic can induce sepsis through inflammation cascade reaction Cytokine Storm (CS). Interleukin (IL)-6, the core of CS, its related signaling pathways have been considered as contributors sepsis. Therefore, it important study relationship between IL-6 sepsis-related diseases. This review generalized mechanism via purpose take rational management for these were sought Kyoto Encyclopedia Genes Genomes (KEGG), retrieved protein-protein interaction Search Interaction tool (STRING). In PubMed Google Scholar, studies searched out, which correlating associating pathological process Focused on interactions pathways, some studied association containing insulin resistance, Alcoholic liver disease (ALD), Alzheimer (AD), atherosclerosis. article summarized inflammatory mechanisms cross-talked other mediators vitro, animal models, human experiments, leading activation accelerating progression The clinicians should be highlight this kind more clinical trials needed provide reliable theoretical basis policy formulation.

Language: Английский

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The potential role of SARS‐CoV‐2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread

Immunity Inflammation and Disease, Journal Year: 2023, Volume and Issue: 11(3)

Published: March 1, 2023

Abstract Coronavirus disease 2019 (COVID‐19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). It has been shown that SARS‐CoV‐2 infection‐induced inflammatory and oxidative stress associated endothelial dysfunction may lead to the development of coronary (ACS). Therefore, this review aimed ascertain link between infection ACS. ACS spectrum myocardial ischemia due sudden decrease in blood flow, ranging from unstable angina infarction (MI). Primary or type 1 MI (T1MI) mainly plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary (T2MI) cardiac systemic disorders without atherothrombotic disruption. Acute linked nonobstructive such as vasospasm, dilated cardiomyopathy, fibrosis, myocarditis. Furthermore, inflammation might affect atherosclerotic stability through augmentation preload afterload. Nevertheless, major vessels plaques develop minor during COVID‐19 since arteries are not initially primarily targeted low expression angiotensin‐converting enzyme vessels. In conclusion, hypercytokinemia, direct cardiomyocyte injury, dysregulation renin‐angiotensin system aggravate underlying cause new‐onset T2MI. As well, arrhythmias induced anti‐COVID‐19 medications could worsen

Language: Английский

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Pharmacological characterization of the antidiabetic drug metformin in atherosclerosis inhibition: A comprehensive insight

Immunity Inflammation and Disease, Journal Year: 2024, Volume and Issue: 12(8)

Published: Aug. 1, 2024

Abstract Background Atherosclerosis (AS) is a progressive disease that interferes with blood flow, leading to cardiovascular complications such as hypertension, ischemic heart disease, stroke, and vascular ischemia. The progression of AS correlated inflammation, oxidative stress, endothelial dysfunction. Various signaling pathways, like nuclear erythroid‐related factor 2 (Nrf2) Kruppel‐like (KLF2), are involved in the pathogenesis AS. Nrf2 KLF2 have anti‐inflammatory antioxidant properties. Thus, activation these pathways may reduce development Metformin, an insulin‐sensitizing drug used management type diabetes mellitus (T2DM), increases expression KLF2. common long‐term macrovascular complication T2DM. metformin, through its pleiotropic effect, attenuate Aims Therefore, this review aims investigate possible role metformin concerning effect on inhibition reactive oxygen species (ROS) formation. In addition antidiabetic can morbidities mortalities compared other agents, even similar glucose control by Nrf2/KLF2 pathway activation. Conclusion conclusion, effective therapeutic strategy against AS, mainly KLF2/Nrf2 axis.

Language: Английский

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Mixed storm in SARS‐CoV‐2 infection: A narrative review and new term in the Covid‐19 era

Immunity Inflammation and Disease, Journal Year: 2023, Volume and Issue: 11(4)

Published: April 1, 2023

Coronavirus disease 2019 (Covid-19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS-CoV-2) leading to the global pandemic worldwide. Systemic complications in Covid-19 are mainly related direct SARS-CoV-2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and development of cytokine storm (CS). As well, developed due propagation oxidative thrombotic events which may progress state called (TS), respectively. In addition, inflammatory lipid storms also activation cells release bioactive lipids correspondingly. Therefore, present narrative review aimed elucidate interrelated relationship between different types mixed (MS). conclusion, infection induces various including CS, storm, TS storm. These not developing alone since there close them. MS seems be more appropriate than it develops intricate interface reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, activated signaling pathway.

Language: Английский

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SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway

Cell Stress and Chaperones, Journal Year: 2023, Volume and Issue: 28(6), P. 657 - 673

Published: Oct. 5, 2023

Coronavirus disease 2019 (COVID-19) is a recent pandemic caused by novel severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) leading to pulmonary and extra-pulmonary manifestations due the development of oxidative stress (OS) hyperinflammation. The underlying cause for OS hyperinflammation in COVID-19 may be related inhibition nuclear factor erythroid 2-related (Nrf2), master regulator antioxidative responses cellular homeostasis. Nrf2 pathway inhibits expression pro-inflammatory cytokines cytokine storm COVID-19. activators can attenuate endothelial dysfunction (ED), renin-angiotensin system (RAS) dysregulation, immune thrombosis, coagulopathy. Hence, this review aimed reveal potential role its management As well, we tried revise mechanistic

Language: Английский

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Dexmedetomidine promotes macrophage cholesterol efflux and prevents atherosclerosis by activating the SIRT1/ABCA1 pathway

Tissue and Cell, Journal Year: 2025, Volume and Issue: unknown, P. 102707 - 102707

Published: Jan. 1, 2025

Language: Английский

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The Peripheral Amyloid-β Nexus: Connecting Alzheimer’s Disease with Atherosclerosis through Shared Pathophysiological Mechanisms

NeuroMolecular Medicine, Journal Year: 2025, Volume and Issue: 27(1)

Published: March 3, 2025

Abstract Alzheimer’s disease (AD) and atherosclerosis (AS) are two chronic diseases with seemingly distinct pathologies. However, emerging research points to a bidirectional relationship driven by common mechanisms, such as inflammation, oxidative stress, dysregulation of Amyloid-Beta (Aβ). This review focuses on the role Aβ critical molecular link between AD AS, emphasizing its contribution neuronal impairment vascular damage. Specifically, peripheral produced in pancreas skeletal muscle tissues exacerbates AS promoting endothelial dysfunction insulin resistance (IR). Furthermore, accelerates progression impairing cerebral blood flow inducing hypoxia, causing accumulation. critically evaluates recent findings, highlighting inconsistencies clinical studies suggesting future directions. Understanding influence could pave way for novel therapeutic approaches targeting shared pathways, particularly clearance inflammation.

Language: Английский

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COVID-19 beyond the lungs: Unraveling its vascular impact and cardiovascular complications—mechanisms and therapeutic implications

Science Progress, Journal Year: 2025, Volume and Issue: 108(1)

Published: Jan. 1, 2025

COVID-19, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), is primarily a illness but significantly affects the cardiovascular system as well. After entering body through tract, directly and indirectly disrupts vascular system. Vascular endothelial cells (ECs), which express ACE2 TMPRSS2, are targets for viral invasion. However, predominant cause of widespread damage “cytokine storm” induced immune response. This leads to EC activation, inflammation, neutrophil neutrophil–platelet aggregation, causing injury. Additionally, increased expression plasminogen activator inhibitor-1 balance between prothrombotic fibrinolytic processes, while activation renin–angiotensin–aldosterone adds oxidative stress endothelium. In heart, SARS-CoV-2 invades ECs, leading apoptosis pyroptosis, exacerbated inflammation elevated catecholamines. These factors contribute arrhythmias, strokes, myocardial infarction in cases COVID-19. narrative review aims explore mechanisms highlight resulting complications. It also identifies research gaps discusses potential therapeutic strategies mitigate impacts

Language: Английский

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Could Acute COVID-19 Infection Ignite Thrombotic Risk?

European Cardiology Review, Journal Year: 2025, Volume and Issue: 20

Published: May 14, 2025

With the growing body of evidence ischaemic and thrombotic risks associated with recent COVID-19 infection, this expert commentary reviews data on cardiovascular risk implications considers potential management approaches for these patients. The authors’ opinions were gauged against a global healthcare professional survey to measure current levels agreement, lending support their validity. While need ongoing research improve understanding disease is appreciated, authors recognise that there transform reduce health impact infection among high-risk patients, especially those established disease.

Language: Английский

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The possible role of nuclear factor erythroid‐2‐related factor 2 activators in the management of Covid‐19

Journal of Biochemical and Molecular Toxicology, Journal Year: 2023, Volume and Issue: 38(1)

Published: Dec. 9, 2023

COVID-19 is caused by a novel SARS-CoV-2 leading to pulmonary and extra-pulmonary manifestations due oxidative stress (OS) development hyperinflammation. primarily asymptomatic though it may cause acute lung injury (ALI), respiratory distress syndrome (ARDS), systemic inflammation, thrombotic events in severe cases. SARS-CoV-2-induced OS triggers the activation of different signaling pathways, which counterbalances this complication. One these pathways nuclear factor erythroid 2-related 2 (Nrf2), induces series cellular interactions mitigate SARS-CoV-2-mediated viral toxicity OS-induced injury. Nrf2 pathway inhibits expression pro-inflammatory cytokines cytokine storm COVID-19. Therefore, activators play an essential role reducing infection-induced inflammation suppressing NLRP3 inflammasome Furthermore, can attenuate endothelial dysfunction (ED), renin-angiotensin system (RAS) dysregulation, immune thrombosis, coagulopathy. Thus mini-review tries clarify possible management could be effective therapeutic strategy Covid-19. Preclinical clinical studies are recommended regard.

Language: Английский

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