ArticleKidney international2020
The transcription factor Twist1 in the distal nephron but not in macrophages propagates aristolochic acid nephropathy.
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 29 citations in OpenAlex.
- Twist2 knockdown alleviates renal ischemia-reperfusion injury by maintaining mitochondrial function and enhancing mitophagy through Bnip3.Human cell · 2025Article
- Identification and analysis of differently expressed transcription factors in aristolochic acid nephropathy.Environmental health and preventive medicine · 2024Article
- Macrophage-derived, LRG1-enriched extracellular vesicles exacerbate aristolochic acid nephropathy in a TGFβR1-dependent manner.Cell biology and toxicology · 2022Article
- Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.JCI insight · 2021Article
- Article
- Obesity Inhibits Angiogenesis Through TWIST1-SLIT2 Signaling.Frontiers in cell and developmental biology · 2021Article
- Upregulation of miR-382 contributes to renal fibrosis secondary to aristolochic acid-induced kidney injury via PTEN signaling pathway.Cell death & disease · 2020Article
- Twist1: A Double-Edged Sword in Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2020Review
- The varying roles of macrophages in kidney injury and repair.Current opinion in nephrology and hypertension · 2020Review
- Aristolochic Acid-Induced Nephrotoxicity: Molecular Mechanisms and Potential Protective Approaches.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tubulointerstitial disease in the kidney culminates in renal fibrosis that portents organ failure. Twist1, a basic helix-loop-helix protein 38 transcription factor, regulates several essential biological functions, but inappropriate Twist1 activity in the kidney epithelium can trigger kidney fibrogenesis and chronic kidney disease. By contrast, Twist1 in circulating myeloid cells may constrain inflammatory injury by attenuating cytokine generation. To dissect the effects of Twist1 in kidney tubular versus immune cells on renal inflammation following toxin-induced renal injury, we subjected mice with selective deletion of Twist1 in renal epithelial cells or macrophages to aristolochic acid-induced chronic kidney disease. Ablation of Twist1 in the distal nephron attenuated kidney damage, interstitial fibrosis, and renal inflammation after aristolochic acid exposure. However, macrophage-specific deletion of Twist1 did not impact the development of aristolochic acid-induced nephropathy. In vitro studies confirmed that Twist1 in renal tubular cells underpins their susceptibility to apoptosis and propensity to generate pro-fibrotic mediators in response to aristolochic acid. Moreover, co-culture studies revealed that Twist1 in renal epithelia augmented the recruitment and activation of pro-inflammatory CD64
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Registered trials
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