Glycolipid Metabolic Disorders, Metainflammation, Oxidative Stress, and Cardiovascular Diseases: Unraveling Pathways

Biology, Год журнала: 2024, Номер 13(7), С. 519 - 519

Опубликована: Июль 12, 2024

Glycolipid metabolic disorders (GLMDs) are various resulting from dysregulation in glycolipid levels, consequently leading to an increased risk of obesity, diabetes, liver dysfunction, neuromuscular complications, and cardiorenal vascular diseases (CRVDs). In patients with GLMDs, excess caloric intake a lack physical activity may contribute oxidative stress (OxS) systemic inflammation. This study aimed review the connection between GLMD, OxS, metainflammation, onset CRVD. GLMD is due causing dysfunction synthesis, breakdown, absorption glucose lipids body, excessive ectopic accumulation these molecules. mainly neuroendocrine dysregulation, insulin resistance, metainflammation. many inflammatory markers defense cells play vital role related tissues organs, such as blood vessels, pancreatic islets, liver, muscle, kidneys, adipocytes, promoting lesions that affect interconnected organs through their signaling pathways. Advanced glycation end products, ATP-binding cassette transporter 1, Glucagon-like peptide-1, Toll-like receptor-4, sphingosine-1-phosphate (S1P) crucial since they glucolipid metabolism. The consequences this system organ damage morbidity mortality.

Язык: Английский

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Cell senescence in liver diseases: pathological mechanism and theranostic opportunity

Nature Reviews Gastroenterology & Hepatology, Год журнала: 2024, Номер 21(7), С. 477 - 492

Опубликована: Март 14, 2024

Язык: Английский

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Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future

Cell Biology and Toxicology, Год журнала: 2024, Номер 40(1)

Опубликована: Март 21, 2024

Abstract Cardiovascular diseases (CVDs) are the main that endanger human health, and their risk factors contribute to high morbidity a rate of hospitalization. Cell death is most important pathophysiology in CVDs. As one cell mechanisms, ferroptosis new form regulated (RCD) broadly participates CVDs (such as myocardial infarction, heart transplantation, atherosclerosis, failure, ischaemia/reperfusion (I/R) injury, atrial fibrillation, cardiomyopathy (radiation-induced cardiomyopathy, diabetes sepsis-induced cardiac doxorubicin-induced iron overload hypertrophic cardiomyopathy), pulmonary arterial hypertension), involving regulation, metabolic mechanism lipid peroxidation. This article reviews recent research on regulation its relationship with occurrence treatment CVDs, aiming provide ideas targets for clinical diagnosis by clarifying latest progress research. Graphical • The identification, development history characterization ferroptosis. role different subcellular organelles organelle-specific regulators includes metabolism, amino acid metabolism. cardiovascular cells diseases. efficacy pathological involved

Язык: Английский

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Endothelial cells under disturbed flow release extracellular vesicles to promote inflammatory polarization of macrophages and accelerate atherosclerosis

BMC Biology, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 21, 2025

Язык: Английский

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The Mechanisms of Sepsis Induced Coagulation Dysfunction and Its Treatment

Journal of Inflammation Research, Год журнала: 2025, Номер Volume 18, С. 1479 - 1495

Опубликована: Фев. 1, 2025

Sepsis is a critical condition characterized by organ dysfunction due to dysregulated response infection that poses significant global health challenges. Coagulation nearly ubiquitous among sepsis patients. Its mechanisms involve platelet activation, coagulation cascade inflammatory reaction imbalances, immune dysregulation, mitochondrial damage, neuroendocrine network disruptions, and endoplasmic reticulum (ER) stress. These factors not only interact but also exacerbate one another, leading severe dysfunction. This review illustrates the of sepsis-induced coagulopathy, with focus on tissue factor endothelial glycocalyx release neutrophil extracellular traps (NETs), all which are potential targets for therapeutic interventions.

Язык: Английский

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A transcriptomic pan-cancer signature for survival prognostication and prediction of immunotherapy response based on endothelial senescence

Journal of Biomedical Science, Год журнала: 2023, Номер 30(1)

Опубликована: Март 28, 2023

The microvascular endothelium inherently controls nutrient delivery, oxygen supply, and immune surveillance of malignant tumors, thus representing both biological prerequisite therapeutic vulnerability in cancer. Recently, cellular senescence emerged as a fundamental characteristic solid malignancies. In particular, tumor endothelial cells have been reported to acquire senescence-associated secretory phenotype, which is characterized by pro-inflammatory transcriptional program, eventually promoting growth formation distant metastases. We therefore hypothesize that (TEC) represents promising target for survival prognostication prediction immunotherapy efficacy precision oncology.Published single-cell RNA sequencing datasets different cancer entities were analyzed cell-specific senescence, before generating pan-cancer senescence-related transcriptomic signature termed EC.SENESCENCE.SIG. Utilizing this signature, machine learning algorithms employed construct response models. Machine learning-based feature selection applied select key genes prognostic biomarkers.Our analyses published indicate variety cancers, exhibit the highest compared or other vascular compartment tumors. Based on these findings, we developed TEC-associated, (EC.SENESCENCE.SIG) positively correlates with pro-tumorigenic signaling, tumor-promoting dysbalance cell responses, impaired patient across multiple entities. Combining clinical data risk score computed from EC.SENESCENCE.SIG, nomogram model was constructed enhanced accuracy prognostication. Towards application, identified three biomarkers probability estimation. As perspective, EC.SENESCENCE.SIG provided superior than previously models.We here established based senescence.

Язык: Английский

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Integrated Cascade Nanozymes with Antisenescence Activities for Atherosclerosis Therapy

Angewandte Chemie International Edition, Год журнала: 2023, Номер 62(33)

Опубликована: Июнь 20, 2023

Senescent cells are the critical drivers of atherosclerosis formation and maturation. Mitigating senescent holds promise for treatment atherosclerosis. In an atherosclerotic plaque microenvironment, interact with reactive oxygen species (ROS), promoting disease development. Here, we hypothesize that a cascade nanozyme antisenescence antioxidant activities can serve as effective therapeutic An integrated superoxide dismutase- glutathione peroxidase-like activities, named MSe1 , is developed in this work. The obtained attenuate human umbilical vein endothelial cell (HUVEC) senescence by protecting DNA from damage. It significantly weakens inflammation macrophages HUVECs eliminating overproduced intracellular ROS. Additionally, effectively inhibits foam decreasing internalization oxidized low-density lipoprotein. After intravenous administration, apolipoprotein E-deficient (ApoE-/- ) mice reducing oxidative stress then decreases infiltration inflammatory plaques. This study not only provides but also suggests combination antioxidative considerable treating

Язык: Английский

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Endothelial cell telomere dysfunction induces senescence and results in vascular and metabolic impairments

Aging Cell, Год журнала: 2023, Номер 22(8)

Опубликована: Май 31, 2023

Abstract In advanced age, increases in oxidative stress and inflammation impair endothelial function, which contributes to the development of cardiovascular disease (CVD). One plausible source this is an increase abundance senescent cells. Cellular senescence a cell cycle arrest that occurs response various damaging stimuli. present study, we tested hypothesis age results telomere dysfunction induces senescence. both human mouse cells, resulted increased dysfunctional telomeres, characterized by activation DNA damage signaling at telomeric DNA. To test whether senescence, selectively reduced shelterin protein repeat binding factor 2 ( Trf2 ) from cells young mice. reduction cellular Furthermore, induction inflammatory stress, resulting impairments function. Finally, demonstrate dysfunction‐induced impairs glucose tolerance. This likely through liver adipose tissue, as well reductions microvascular density vasodilation metabolic Cumulatively, findings study identify age‐related mechanism leads these data provide compelling evidence contribute arterial

Язык: Английский

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The impact of cellular senescence in human adipose tissue

Journal of Cell Communication and Signaling, Год журнала: 2023, Номер 17(3), С. 563 - 573

Опубликована: Май 17, 2023

Abstract In the last decades prevalence of obesity has increased dramatically, and worldwide epidemic related metabolic diseases contributed to an interest for adipose tissue (AT), primary site storage lipids, as a metabolically dynamic endocrine organ. Subcutaneous AT is depot with largest capacity store excess energy when its limit reached hypertrophic obesity, local inflammation, insulin resistance ultimately type 2 diabetes (T2D) will develop. Hypertrophic also associated dysfunctional adipogenesis, depending on inability recruit differentiate new mature cells. Lately, cellular senescence (CS), aging mechanism defined irreversible growth arrest that occurs in response various stressors, such telomere shortening, DNA damage oxidative stress, gained lot attention regulator tissues aging-associated conditions. The abundance senescent cells increases not only but independent age. Senescent characterized by cells, decreased sensitivity lipid storage. resident progenitor (APC), non-proliferating microvascular endothelial are affected burden. Dysfunctional APC have both impaired adipogenic proliferative capacity. Interestingly, human from obese hyperinsulinemic individuals been shown re-enter cell cycle senesce, which indicates endoreplication. CS was found be more pronounced T2D individuals, compared matched non-diabetic Graphical abstract Factors

Язык: Английский

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A framework of biomarkers for vascular aging: a consensus statement by the Aging Biomarker Consortium

Life Medicine, Год журнала: 2023, Номер 2(4)

Опубликована: Авг. 30, 2023

Aging of the vasculature, which is integral to functioning literally all human organs, serves as a fundamental physiological basis for age-related alterations well shared etiological mechanism various chronic diseases prevalent in elderly population. China, home world's largest aging population, faces an escalating challenge addressing prevention and management these conditions. To meet this challenge, Biomarker Consortium China has developed expert consensus on biomarkers vascular (VA) by synthesizing literature insights from scientists clinicians. This provides comprehensive assessment associated with VA presents systemic framework classify them into three dimensions: functional, structural, humoral. Within each dimension, panel recommends most clinically relevant biomarkers. For functional domain, reflecting stiffness endothelial function are highlighted. The structural dimension encompasses metrics structure, microvascular distribution. Additionally, proinflammatory factors emphasized humoral dimension. aim establish foundation assessing extent conducting research related VA, ultimate goal improving health globally.

Язык: Английский

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