Cited by Role of mitophagy in intervertebral disc degeneration: A narrative review

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

Enzo Pereira de Lima,

Renato Cesar Moretti,

Karina Torres Pomini

et al.

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

Citations

VEGFR3 mitigates hypertensive nephropathy by enhancing mitophagy via regulating crotonylation of HSPA1L DOI

Q Wu,

Jiaxin Fu,

Bin Zhu

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Jan. 28, 2025

Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect VEGFR3 in salt-sensitive hypertension. However, specific mechanism underlying role kidney during overactivation renin-angiotensin-aldosterone system remains unclear. In present study, nephropathy was established by angiotensin II (Ang II). found that highly increased PTCs Ang II-infused mice. Activation mitigated dysfunction, pathological damage, and oxidative stress II-induced Moreover, we restored mitophagy deficiency induced both vivo vitro to alleviate injury PTCs. Furthermore, experiment demonstrated improved abnormal enhancing PARKIN mitochondrial translocation. LC-MS/MS Co-IP assays identified HSPA1L as interacted protein VEGFR3, which promoted translocation PARKIN. Mechanistically, disorder domain bound HSPA1L, crotonylation modification at K130 required for regulation context Finally, on were attenuated transfection (HSPA1L-K130R) mutant plasmid vitro. These findings indicated alleviated promoting PARKIN-dependent pathway via regulating site PTCs, provided a mechanistic basis therapeutic target

Language: Английский

Citations

Knocking Down EGR1 Inhibits Nucleus Pulposus Cell Senescence and Mitochondrial Damage through Activation of PINK1-Parkin Dependent Mitophagy, Thereby Delaying Intervertebral Disc Degeneration DOI

Zuolong Wu,

Ke-Ping Wang,

Yajun Chen

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 224, P. 9 - 22

Published: Aug. 14, 2024

Language: Английский

Citations

The Significance of Cellular Senescence Hub Genes in the Diagnosis and Subtype Classification of a Comprehensive Database of Gene Expression in Intervertebral Disc Degeneration DOI

Fei Liu,

Silong Gao,

Yin Ji

et al.

JOR Spine, Journal Year: 2025, Volume and Issue: 8(1)

Published: March 1, 2025

Intervertebral disc degeneration (IVDD) is a complex age-related physiological process, with cellular senescence (CS) being primary contributing factor. However, the precise role of CS and its associated genes in IVDD remains unclear. In this study, we performed differential expression analysis on GSE124272 GSE150408 datasets from GEO database identified 53 differentially expressed senescence-related (CSRGs). We then conducted Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analyses to explore their functions pathways. hub by constructing protein-protein interaction (PPI) network further validated these using clinical samples. explored functional prognostic significance support vector machine recursive feature elimination (SVM-RFE), random forest (RF), least absolute shrinkage selection operator (LASSO) algorithms. visualized correlation between levels four core immune cell infiltration heat maps histograms. Finally, graphene oxide 297 (DEGs) investigate IVDD. ultimately CSRGs DUSP3, MAPKAPK5, SP1, VEGFA, various algorithms Our results revealed that DUSP3 SP1 were upregulated IVDD, while MAPKAPK5 VEGFA downregulated. Immune demonstrated positively correlated levels, whereas negatively correlated. summary, play an important pathogenesis our study gene cluster may guide future therapeutic strategies for

Language: Английский

Citations

Role of oxidative stress in intervertebral disc degeneration: mechanisms, pathogenesis, and therapeutic strategies DOI