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

Biology, Journal Year: 2024, Volume and Issue: 13(7), P. 519 - 519

Published: July 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.

Language: Английский

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Regulation of cellular and systemic sphingolipid homeostasis

Nature Reviews Molecular Cell Biology, Journal Year: 2024, Volume and Issue: 25(10), P. 802 - 821

Published: June 18, 2024

Language: Английский

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MSCs Suppress Macrophage Necroptosis and Foster Liver Regeneration by Modulating SP1/SK1 Axis in Treating Acute Severe Autoimmune Hepatitis

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 3, 2025

Abstract Acute severe autoimmune hepatitis (AS‐AIH) is characterized by rapid progression and poor prognosis, with a current lack of effective targeted treatments. Stem cell therapy has demonstrated significant therapeutic promise across various diseases. However, the intricate pathogenesis AS‐AIH hindered widespread utilization mesenchymal stem cells (MSCs) in this domain. Herein, it that necroptosis, as primary mode death AIH, crucial causing AS‐AIH. Inflammatory macrophages are population involved necroptosis. Inhibition specificity protein 1/sphingosine kinase 1/sphingosine‐1‐phosphate (SP1/SK1/S1P) axis responsible for phenomenon, leading to excessive activation intrahepatic immune system aggravating liver damage. Furthermore, S1P/S1PR2/YAP key pathway initiating regeneration during S1P synthesized hepatocytes source, process also regulated SP1/SK1 axis. MSCs promote synthesis through delivery SP1, which inhibits necroptosis synergistically enhances regeneration. In addition, same mechanism, further aiding These findings unveil core provide theoretical foundation using potential modality.

Language: Английский

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Cardiac Regeneration in Adult Zebrafish: A Review of Signaling and Metabolic Coordination

Current Cardiology Reports, Journal Year: 2025, Volume and Issue: 27(1)

Published: Jan. 10, 2025

Language: Английский

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Absolute Quantitative Lipidomics Reveals Differences in Lipid Compounds in the Blood of Trained and Untrained Yili Horses

Veterinary Sciences, Journal Year: 2025, Volume and Issue: 12(3), P. 255 - 255

Published: March 10, 2025

The purpose of this study was to explore the relationship between blood lipid levels and differences in cardiac structure function trained untrained Yili horses as related exercise performance. We utilized quantitative lipidomics technology elucidate how compounds influenced performance outcomes. Sixteen 18-month-old were selected, ten which received a 15-week training regimen, six kept controls. Cardiac assessed by echocardiography, while plasma metabolites detected identified liquid chromatography–mass spectrometry. results showed that key structural indices, such left ventricular end-diastolic diameter, end-systolic posterior wall thickness, significantly greater group compared with group, indicating promotes adaptive remodeling. Regarding metabolites, significant observed groups, total 281 lipids identified—212 upregulated 69 downregulated. These differentially expressed primarily enriched pathways necroptosis, ether metabolism, sphingolipid signaling, are associated cell migration, survival, proliferation, regulation metabolism. Further correlation analysis revealed certain lipids, PE (20:4_18:0), PC (17:0_18:1), LPC subclasses, correlated exercise-mediated functional changes enhancement. findings provide novel molecular insights into effects on metabolism can serve reference for strategies preserving health horses.

Language: Английский

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KLF1 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through Regulation of Wnt/β‐Catenin Signaling Pathway

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: March 27, 2025

Innovative therapeutic approaches for heart failure, a leading cause of mortality worldwide, are urgently needed. In this study, the important role Krüppel-like factor 1 (KLF1) in cardiomyocyte proliferation and regeneration is explored, revealed its ability to regulate Wnt/β-catenin signaling pathway as well exploring feasible strategy target KLF1 treatment failure. Postnatally, marked decrease expression occurred almost simultaneously with reduction myocardial regenerative capacity. Through comprehensive vivo vitro studies, it demonstrated that neonatal adult mice, overexpression significantly increased promoted repair following infarction, whereas knockout abolished these effects. Mechanistically, through RNA sequencing (RNA-seq) ATAC (ATAC-seq) analyses, promotion by associated pathway, mitochondrial function, fatty acid metabolism. These findings highlight regeneration, which provides novel insights into targets

Language: Английский

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Glycerophospholipid and Sphingosine- 1-phosphate Metabolism in Cardiovascular Disease: Mechanisms and Therapeutic Potential

Journal of Cardiovascular Translational Research, Journal Year: 2025, Volume and Issue: unknown

Published: April 14, 2025

Language: Английский

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Metformin alleviates sphingolipids dysregulation and improves obesity-related kidney disease in high fat diet rats

Journal of Pharmacology and Experimental Therapeutics, Journal Year: 2025, Volume and Issue: 392(3), P. 103388 - 103388

Published: Jan. 17, 2025

Obesity-related kidney disease (ORKD) has recently become a global health issue. Metformin is widely used in patients with type 2 diabetes concomitant obesity, but its effects on ORKD are insufficiently understood. Accumulation of lipid species including sphingolipids been reported to disrupt glomerular functions and drive progression chronic disease. The present study aimed test the hypothesis that metformin could exert beneficial ORKD, which may be associated changes renal lipidomics. Male Sprague-Dawley rats were divided into normal chow diet (ND) group or high-fat (HFD)-fed group. After 8 weeks, HFD-fed was subdivided treatment (HFD-Met) control (HFD-C) for an additional weeks. Sphingolipids phospholipids cortex measured by targeted Compared ND group, HFD-C developed histopathological features ORKD. alleviated dyslipidemia, dysfunction, proteinuria, hypertrophy, podocyte damage, fibrosis rats. Renal sphingolipid analysis showed elevations total ceramide, sphingosine, glucosylceramide, galactosylceramide levels versus Specific species, such as ceramide d18:1/22:0, glucosylceramide d18:1/20:0, d18:1/16:0, positively oxidative stress insulin resistance, reduced HFD-Met phospholipid increased phosphatidylcholine lysophosphatidylcholine (LPC) ratio saturated monounsaturated LPCs polyunsaturated significantly These results suggest alleviates dysregulation improves SIGNIFICANCE STATEMENT: To date, this first report explore findings reveal specific crucial deeper understanding underlying mechanisms obesity-related it. signature have significant implications developing therapeutic strategies

Language: Английский

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Blood-borne sphingosine 1-phosphate maintains vascular resistance and cardiac function.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 19, 2025

Abstract G protein-coupled receptors (GPCRs) are key regulators of cardiovascular function that provide targets for the treatment disease. Sphingosine 1-phosphate (S1P) is an erythrocyte- and platelet-derived lipid mediator with cognate GPCRs on endothelial cells (EC), vascular smooth muscle (VSMC) cardiomyocytes. S1P circulates in plasma bound to apolipoprotein M (ApoM)-containing high-density lipoproteins (HDL) albumin. Circulating levels correlate positively systolic blood pressure hypertension negatively severity septic shock left ventricular (LV) coronary heart In mice, impaired binding HDL or signaling EC both trigger hypertension, supporting essential role HDL-S1P function. The roles albumin-S1P myocyte S1PRs homeostasis remain incompletely defined. Contrasting isolated deficiency, we report non-selective depletion circulating pools mice impairs LV contractile induces hypotension resistance spontaneous increase age. Cardiac output was preserved naïve deficient by compensatory dilation, but cardiac reserve reduced a dobutamine stress test. These phenotypes tracked hematopoietic cell production were partially fully reversed erythrocyte transfusion. Hypotension accompanied peripheral resistance, infusion dose-dependently increased perfused kidneys from wild-type not compound deficiency S1PR2&3. Epistatic analysis supported critical S1PR3 S1P-dependent regulation pointed distinct origin phenotype. Although elevated hypertensive humans, increasing sufficient induce naive mice. observations suggests crosses endothelium arteries gain access VSMC receptors, S1PR maintenance They also highlight chaperones specifying responses relevance as biomarker potential therapeutic target failure.

Language: Английский

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Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair

Frontiers in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 12

Published: Feb. 7, 2025

Cardiovascular diseases are the most lethal worldwide, of which myocardial infarction is leading cause death. After infarction, in order to ensure normal blood supply heart, remaining cardiomyocytes compensate for loss mainly by working at high capacity rather than proliferating produce new cardiomyocytes. This partly due extremely limited ability adult heart repair itself. A growing body research suggests that cardiac regenerative closely related metabolic shifts energy sources. Currently, a large number studies have focused on changes levels before and after proliferation window cardiomyocytes, so it crucial search relevant factors pathways regulate cell cycle cardiomyocyte progression. paper presents review role metabolism injury. It aims elucidate effects mammals point out directions regeneration clinical treatment infarction.

Language: Английский

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