Acetylation of FOXO1 is involved in cadmium-induced rat kidney injury via mediating autophagosome-lysosome fusion blockade and autophagy inhibition DOI Creative Commons

Yingxin Ruan,

Yang Xue, Pengyu Zhang

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 287, P. 117253 - 117253

Published: Nov. 1, 2024

Cadmium (Cd), a potentially toxic elements, has the potential to cause harm kidneys. Studies demonstrated that autophagosome-lysosome fusion blockade and consequent autophagy inhibition is related Cd-induced kidney injury. indicate acetylation of forkhead box protein O1 (FOXO1) as transcriptional factor lysosomal genes, but its roles in Cd-exposed tissues remains unclear till now. Therefore, present study was conducted elucidate this issue. Data found Cd enhances level FOXO1 inhibits expression silent information regulator 1 (Sirt1, deacetylase FOXO1). Pharmacological activation Sirt1 (SRT2104 treatment) decreases Cd-increased FOXO1, Cd-inhibited transcription Ras-related 7 (Rab7), restores Cd-blocked autophagosome lysosome, alleviates inhibition. Moreover, data corroborated inhibiting conductive mitigating Collectively, these results demonstrate mediates during injury, while regulating may be mechanism treating nephrotoxicity after exposure.

Language: Английский

The interplay between osteoarthritis and osteoporosis: Mechanisms, implications, and treatment considerations – A narrative review DOI Creative Commons
Kai Huang,

Haili Cai

Experimental Gerontology, Journal Year: 2024, Volume and Issue: 197, P. 112614 - 112614

Published: Oct. 23, 2024

Language: Английский

Citations

4
Apoptotic vesicles derived from bone marrow mesenchymal stem cells increase angiogenesis in a hind limb ischemia model via the NAMPT/SIRT1/FOXO1 axis DOI Creative Commons
Jinxing Chen,

Zekun Shen,

Bingyi Chen

et al.

Stem Cell Research & Therapy, Journal Year: 2025, Volume and Issue: 16(1)

Published: March 1, 2025

Abstract Background Chronic limb-threatening ischemia (CLTI) is the most severe form of peripheral arterial disease (PAD). Mesenchymal stem cell (MSC) transplantation holds promise as a treatment for CLTI; however, harsh local environment poses challenges to its effectiveness. Apoptotic vesicles (ApoVs) are extracellular produced by cells undergoing apoptosis, and they can carry various biomolecules from their parent cells, including proteins, RNA, DNA, lipids, ions, gas neurotransmitters. ApoVs play significant roles in anti-inflammatory responses, anti-tumor activities, tissue regeneration through intercellular communication, have demonstrated potential drug carriers. In this study, we investigated bone marrow (BMSC)-derived treating CLTI. Methods vivo, explored therapeutic effect on hindlimb model Laser Doppler, matrigel plug assay, histological analysis. vitro, analyzed effects proliferation, migration, angiogenesis HUVECs uptake process ApoVs. addition, Proteomic analysis, western blotting, quantitative real-time PCR, shRNA, siRNA were used analyze ApoVs-induced activation downstream signaling pathways. Results BMSCs showed improvement hind limb model, still exists after apoptosis BMSCs. Subsequently, isolated found improve mouse vivo. be ingested dynamin-, clathrin-, caveolin-mediated endocytosis promote angiogenesis. Mechanistically, transferred NAMPT HUVECs, therefore activating NAMPT/SIRT1/FOXO1 axis, influencing transcriptional activity FOXO1, promoting Conclusions Our results demonstrate that transplanted ameliorate releasing during apoptosis. The main mechanism axis. This study provides different insights into mechanisms suggests promising direction transplantation. Clinical trial number Not applicable. Graphical

Language: Английский

Citations

0
Remimazolam alleviates hepatic ischemia-reperfusion injury by activating FOXO1/3 signaling DOI Creative Commons
Bo Zhou, Jian Liu, Lü Jin

et al.

BMC Gastroenterology, Journal Year: 2025, Volume and Issue: 25(1)

Published: April 22, 2025

Hepatic ischemia reperfusion injury (HIRI) frequently gives rise to aggravated liver damage. Currently, there exists a diverse range of anesthetic drugs that possess protective capabilities against ischemia-reperfusion (IRI). Nevertheless, the specific functions and underlying mechanisms remimazolam (RMZL) in HIRI have not been fully elucidated. models both hepatocytes mice were successfully established. To evaluate function injury, ELISA, HE TUNEL staining employed. The levels oxidative stress markers inflammatory factors measured using commercial kits. Cell viability apoptosis by CCK-8 flow cytometry, respectively. abundance genes proteins was determined utilizing RT-qPCR western blot. It observed RMZL administration greatly alleviated damage repressed inflammation mouse models. In vitro experiments demonstrated strongly protected LO2 cells from H/R-induced cell damage, stress, responses. Moreover, FOXO1 FOXO3, which as classic protection anti-oxidative factors, be downregulated tissue H/R-challenged cells. Notably, this downregulation could reversed RMZL. Furthermore, or FOXO3 knockdown abolished effects RMZL, including promoted survival inhibited upon H/R exposure. These data provided robust support for notion attenuated alleviate through enhancing expressions, suggesting holds great promise potential candidate treatment.

Language: Английский

Citations

0
Acetylation of FOXO1 is involved in cadmium-induced rat kidney injury via mediating autophagosome-lysosome fusion blockade and autophagy inhibition DOI Creative Commons

Yingxin Ruan,

Yang Xue, Pengyu Zhang

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 287, P. 117253 - 117253

Published: Nov. 1, 2024

Cadmium (Cd), a potentially toxic elements, has the potential to cause harm kidneys. Studies demonstrated that autophagosome-lysosome fusion blockade and consequent autophagy inhibition is related Cd-induced kidney injury. indicate acetylation of forkhead box protein O1 (FOXO1) as transcriptional factor lysosomal genes, but its roles in Cd-exposed tissues remains unclear till now. Therefore, present study was conducted elucidate this issue. Data found Cd enhances level FOXO1 inhibits expression silent information regulator 1 (Sirt1, deacetylase FOXO1). Pharmacological activation Sirt1 (SRT2104 treatment) decreases Cd-increased FOXO1, Cd-inhibited transcription Ras-related 7 (Rab7), restores Cd-blocked autophagosome lysosome, alleviates inhibition. Moreover, data corroborated inhibiting conductive mitigating Collectively, these results demonstrate mediates during injury, while regulating may be mechanism treating nephrotoxicity after exposure.

Language: Английский

Citations

0