Erbin Regulates Tissue Factors Through Ras/Raf Pathway in Coagulation Disorders in Sepsis

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 1739 - 1754

Published: Feb. 1, 2025

Background: Sepsis, as a clinically critical disease, usually induces coagulation disorders. It has been reported that ERBB2 Interacting Protein (Erbin) is involved in the development of various inflammatory diseases, and macrophages are regulation disorders sepsis. However, role Erbin sepsis relationship between macrophage function still unclear. Methods: At cellular level, were treated with lipopolysaccharide (LPS) or MEK inhibitor (PD98059), protein expression levels detected by Western blot, co-immunoprecipitation (Co-IP), immunofluorescence, mRNA quantitative real-time polymerase chain reaction (qPCR), concentration tissue factor (TF) cell supernatant was enzyme linked immunosorbent assay (ELISA). animal cecal ligation perforation (CLP) model constructed mice, response disorder mice observed hematoxylin-eosin (HE) staining, immunohistochemistry, ELISA, automatic hemagglutination analyzer. The level blot qPCR. Pearson linear correlation analysis used to analyze inflammation index index. Results: We confirmed plays In vivo studies have shown deletion more obvious enhanced function, vitro knockout mediated secretion TF activating Ras/Raf pathway. Conclusion: reduces activation inhibiting release from macrophages. Keywords: Erbin, disorders, sepsis, factor,

Language: Английский

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Current Evidence and Therapeutic Implications of PANoptosis in Sepsis

Advances in Clinical Medicine, Journal Year: 2025, Volume and Issue: 15(03), P. 2490 - 2504

Published: Jan. 1, 2025

Language: Английский

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5'tiRNA-33-CysACA-1 promotes septic cardiomyopathy by targeting PGC-1α-mediated mitochondrial biogenesis

The International Journal of Biochemistry & Cell Biology, Journal Year: 2024, Volume and Issue: 179, P. 106714 - 106714

Published: Dec. 2, 2024

Language: Английский

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High-Throughput Screening of an FDA-Approved Compound Library Reveals a Novel GAS6 Receptor Agonist for Therapeutic Intervention in Septic Myocardial and microvascular Injury via Modulation of Danger-Associated Molecular Patterns

International Journal of Biological Sciences, Journal Year: 2024, Volume and Issue: 20(15), P. 6222 - 6240

Published: Nov. 11, 2024

PGAM5 and VDAC1 have both been reported to regulate mitophagy. However, the mechanisms by which they sepsis-induced inflammatory microvascular injury remain unverified. In previous studies, we established role of this regulatory axis in various phenotypic processes, including mitophagy, mitochondrial biogenesis, unfolded protein response, dynamics, while further confirming interactive proteins within axis. validation elucidation these phenotypes primarily focused on ischemic heart diseases such as myocardial failure. Sepsis-related is currently recognized a significant cardiac impairment, although there are cardioprotective nutritional agents available for supportive therapy, fundamental research validating upstream targets still lacking. Based our research, explored mitophagy dysfunction mediated its coronary injury. We also confirmed material basis metabolic pathway regulation targeting PGAM5- mechanism with relevant drugs. Our findings suggest that PGAM5-mediated may be crucial factor leading injury, interacting VDAC1-mediated membrane dysfunction. Animal experiments revealed cardiac-specific knockout could reverse LPS-induced damage, restoring ejection function functionality. vitro studies PGAM5-VDAC1 interaction can normalize normal morphology structure mitochondria maintaining energy metabolism levels respiratory chain function. Further pharmacological indicated active ingredients traditional Chinese medicine-Puerarin (TCM, GAS6 Receptor Agonist) target inhibit necrotic apoptosis cardiomyocytes, potentially reversing pathway-related TCM emerge prospective therapeutic agent

Language: Английский

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RIP1 inhibition reduces chondrocyte apoptosis through downregulating nuclear factor-kappa B signaling in a mouse osteoarthritis model

Molecular Biology Reports, Journal Year: 2024, Volume and Issue: 51(1)

Published: Nov. 8, 2024

Language: Английский

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