ArticleJournal of the American Society of Nephrology : JASN2017
Inhibition of Reticulon-1A-Mediated Endoplasmic Reticulum Stress in Early AKI Attenuates Renal Fibrosis Development.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 71 citations in OpenAlex.
- O-Glycosylation of E-Cadherin Induced by Endoplasmic Reticulum Stress Negatively Regulates Cell Polarity and Proliferation in Acute Kidney Injury.Journal of biochemical and molecular toxicology · 2026Article
- Caveolin-1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Influence of Sex and Hormones on Organelle Stress in Kidney Injury: Insights from Preclinical Models.Biology · 2026Review
- The multiple roles of Ggt1-Cre in the generation of transgenic mice.Cellular & molecular biology letters · 2026Article
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- SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RTN1A mediates diabetes-induced AKI-to-CKD transition.JCI insight · 2024Article
- Cisplatin Nephrotoxicity Is Critically Mediated by the Availability of BECLIN1.International journal of molecular sciences · 2024Article
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Inhibition of MiR-106b-5p mediated by exosomes mitigates acute kidney injury by modulating transmissible endoplasmic reticulum stress and M1 macrophage polarization.Journal of cellular and molecular medicine · 2023Article
- Toll-like receptors 2 and 4 stress signaling and sodium-glucose cotransporter-2 in kidney disease.Molecular and cellular biochemistry · 2023Review
- Research progress on endoplasmic reticulum homeostasis in kidney diseases.Cell death & disease · 2023Review
- Vitamin D receptor attenuate ischemia-reperfusion kidney injury via inhibiting ATF4.Cell death discovery · 2023Article
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- Tubular cells produce FGF2 via autophagy after acute kidney injury leading to fibroblast activation and renal fibrosis.Autophagy · 2023Article
- Targeting Endoplasmic Reticulum for Novel Therapeutics and Monitoring in Acute Kidney Injury.Nephron · 2023Review
- A novel contrast-induced acute kidney injury mouse model based on low-osmolar contrast medium.Renal failure · 2022Article
- Emerging links between endoplasmic reticulum stress responses and acute kidney injury.American journal of physiology. Cell physiology · 2022Review
- Impaired fatty acid metabolism perpetuates lipotoxicity along the transition to chronic kidney injury.JCI insight · 2022Article
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Several animal studies have shown an important role for endoplasmic reticulum (ER) stress in AKI, whereas human studies are lacking. We recently reported that Reticulon-1A (RTN1A) is a key mediator of ER stress and kidney cell injury. Here, we investigated whether modulation of RTN1A expression during AKI contributes to the progression to CKD. In a retrospective study of 51 patients with AKI, increased expression of RTN1A and other ER stress markers were associated with the severity of kidney injury and with progression to CKD. In an inducible tubular cell-specific RTN1A-knockdown mouse model subjected to folic acid nephropathy (FAN) or aristolochic acid nephropathy, reduction of RTN1A expression during the initial stage of AKI attenuated ER stress and kidney cell injury in early stages and renal fibrosis development in later stages. Treatment of wild-type mice with tauroursodeoxycholic acid, an inhibitor of ER stress, after the induction of kidney injury with FA facilitated renoprotection similar to that observed in RTN1A-knockdown mice. Conversely, in transgenic mice with inducible tubular cell-specific overexpression of RTN1A subjected to FAN, induction of RTN1A overexpression aggravated ER stress and renal injury at the early stage and renal fibrosis at the late stage of FAN. Together, our human and mouse data suggest that the RTN1A-mediated ER stress response may be an important determinant in the severity of AKI and maladaptive repair that may promote progression to CKD.
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