The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway DOI Open Access
Lei Yang,

K GONG,

Guosheng Ren

et al.

Biotechnology and Applied Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 22, 2024

Osteoarthritis (OA) is a degenerative joint disorder characterized by progressive cartilage degradation. Excessive oxidative stress (OS), inflammatory responses, extracellular matrix breakdown, and cellular senescence of chondrocytes play crucial roles in the pathological development OA. Currently, curing OA remains significant challenge. In this study, we aimed to elucidate protective effects Annexin A1 protein Mimetic Peptide (Ac2-26) against tumor necrosis factor-α (TNF-α)-induced damage CHON-001 assessing senescence, OS, expression levels metalloproteinase-13 (MMP-13) disintegrin metalloproteinase with thrombospondin motifs (ADAMTS)-4. Our results show that Ac2-26 mitigated reduction telomerase activity exacerbation induced TNF-α chondrocytes. Treatment led decreased human reverse transcriptase gene increased telomeric repeat-binding factor 2 gene, which were reversed treatment. The TNF-α-induced increases expressions p53 p16 restored dose-dependent manner. Additionally, found caused elevations mRNA MMP-13 ADAMTS-4, reduced fashion. Furthermore, triggered activation nuclear κ-B (NF-κB) increasing phosphorylated NF-κB p65 luciferase NF-κB. Notably, alleviated OS reducing mitochondrial reactive oxygen species promoting NF-E2-related (Nrf2) TNF-α-challenged Silencing Nrf2 abolished Ac2-26-induced Collectively, these findings offer new insights into potential therapeutic use for treating

Language: Английский

What do You Need to Know after Diabetes and before Diabetic Retinopathy? DOI Creative Commons
Shiyu Zhang, Jia‐Ren Liu, Heng Zhao

et al.

Aging and Disease, Journal Year: 2025, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2025

Diabetic retinopathy (DR) is a leading cause of vision impairment and blindness among individuals with diabetes mellitus. Current clinical diagnostic criteria mainly base on visible vascular structure changes, which are insufficient to identify diabetic patients without DR (NDR) but dysfunctional retinopathy. This review focuses retinal endothelial cells (RECs), the first sense respond elevated blood glucose. As glucose rises, RECs undergo compensatory transitional phases, correspondingly altered molecules likely become biomarkers targets for early prediction treatment NDR article elaborated possible pathophysiological processes focusing summarized recently published reliable screening emerging intervention strategies Additionally, references medication selection lifestyle recommendations this population provided. aims deepen understanding REC biology pathophysiology, emphasizes importance detection intervention, points out future directions improve diagnosis reduce occurrence DR.

Language: Английский

Citations

0
Glis1 inhibits RTEC cellular senescence and renal fibrosis by downregulating histone lactylation in DKD DOI
Juan Chen, Junling He, Xiaoyue Wang

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: unknown, P. 123293 - 123293

Published: Dec. 1, 2024

Language: Английский

Citations

3
The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway DOI Open Access
Lei Yang,

K GONG,

Guosheng Ren

et al.

Biotechnology and Applied Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 22, 2024

Osteoarthritis (OA) is a degenerative joint disorder characterized by progressive cartilage degradation. Excessive oxidative stress (OS), inflammatory responses, extracellular matrix breakdown, and cellular senescence of chondrocytes play crucial roles in the pathological development OA. Currently, curing OA remains significant challenge. In this study, we aimed to elucidate protective effects Annexin A1 protein Mimetic Peptide (Ac2-26) against tumor necrosis factor-α (TNF-α)-induced damage CHON-001 assessing senescence, OS, expression levels metalloproteinase-13 (MMP-13) disintegrin metalloproteinase with thrombospondin motifs (ADAMTS)-4. Our results show that Ac2-26 mitigated reduction telomerase activity exacerbation induced TNF-α chondrocytes. Treatment led decreased human reverse transcriptase gene increased telomeric repeat-binding factor 2 gene, which were reversed treatment. The TNF-α-induced increases expressions p53 p16 restored dose-dependent manner. Additionally, found caused elevations mRNA MMP-13 ADAMTS-4, reduced fashion. Furthermore, triggered activation nuclear κ-B (NF-κB) increasing phosphorylated NF-κB p65 luciferase NF-κB. Notably, alleviated OS reducing mitochondrial reactive oxygen species promoting NF-E2-related (Nrf2) TNF-α-challenged Silencing Nrf2 abolished Ac2-26-induced Collectively, these findings offer new insights into potential therapeutic use for treating

Language: Английский

Citations

1