ArticleInflammation2025
Inhibition of SLC3A2 Deletion-Mediated Ferroptosis by Bone Marrow Stromal Cells to Alleviate Inflammation and Fibrosis in Diabetic Kidney Disease.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- The progress and challenges of mesenchymal stromal cell-based therapy for diabetes and its complications.Biological research · 2026Review
- Iron-Driven Ferroptosis in Diabetic Kidney Disease: From Molecular Mechanisms to Targeted Therapeutic Translation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Pathogenesis and Therapeutic Perspectives of Tubular Injury in Diabetic Kidney Disease: An Update.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Renal fibrosis and inflammatory infiltration are common pathological features of diabetic kidney disease (DKD). Bone marrow mesenchymal stem cells (BMSCs) are recognized for their anti-fibrotic and anti-inflammatory properties. The objective of this study was to assess the effects of BMSCs on DKD and elucidate their potential mechanisms of action. To assess the role of BMSCs, a DKD model was induced in Sprague-Dawley (SD) rats using streptozotocin (STZ) combined with a high-fat diet, and a human kidney-2 (HK-2) cell damage model was established using high glucose. To investigate the mechanism of the impact of BMSCs on DKD at the genetic level, transcriptome sequencing of the treated HK-2 cells was conducted, identifying the differentially expressed gene SLC3A2, which is related to ferroptosis. A HK-2 cell damage model with SLC3A2 knockout was then constructed to assess the effects of BMSCs on ferroptosis, inflammation, and fibrosis. Also, the potential relationship between BMSCs and the mitogen-activated protein kinase (MAPK) signaling pathway was assessed. In vivo and in vitro studies demonstrated that BMSCs enhanced inflammation and fibrosis in DKD by inhibiting ferroptosis. Knockdown of SLC3A2 promoted ferroptosis, inflammation, and fibrosis, while BMSCs reversed these effects, likely through the inhibition of the MAPK signaling pathway. This research demonstrated that ferroptosis and the activation of the MAPK signaling pathway can promote the onset and progression of DKD. It revealed the therapeutic role of BMSCs in DKD treatment and proposed that SLC3A2 might serve as a potential target for DKD therapy, thereby providing a theoretical foundation for the treatment of DKD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.