ArticleWorld journal of diabetes2024
β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy.
Article in World journal of diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- Exploring a novel mechanism for targeting β-arrestin-2 in the management of diabetic nephropathy.World journal of diabetes · 2025Article
- From metabolic regulation to kidney protection: β-arrestin 2 as a dual-function therapeutic target.World journal of diabetes · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
backgroundGlomerular endothelial cell (GENC) injury is a characteristic of early-stage diabetic nephropathy (DN), and the investigation of potential therapeutic targets for preventing GENC injury is of clinical importance.
aimTo investigate the role of β-arrestin-2 in GENCs under DN conditions.
methodsEight-week-old C57BL/6J mice were intraperitoneally injected with streptozotocin to induce DN. GENCs were transfected with plasmids containing siRNA-β-arrestin-2, shRNA-activating transcription factor 6 (ATF6), pCDNA-β-arrestin-2, or pCDNA-ATF6. Additionally, adeno-associated virus (AAV) containing shRNA-β-arrestin-2 was administered
resultsThe upregulation of β-arrestin-2 was observed in patients with DN as well as in GENCs from DN mice. Knockdown of β-arrestin-2 reduced apoptosis in high glucose-treated GENCs, which was reversed by the overexpression of ATF6. Moreover, overexpression of β-arrestin-2 Led to the activation of endoplasmic reticulum (ER) stress and the apoptosis of GENCs which could be mitigated by silencing of ATF6. Furthermore, knockdown of β-arrestin-2 by the administration of AAV-shRNA-β-arrestin-2 alleviated renal injury in DN mice.
conclusionKnockdown of β-arrestin-2 prevents GENC apoptosis by inhibiting ATF6-mediated ER stress
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