ArticleNature communications2023
Intrinsic TGF-β signaling attenuates proximal tubule mitochondrial injury and inflammation in chronic kidney disease.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Transforming growth factor-β in kidney disease in dogs and cats: a review of the evidence of its role in renal fibrosis.Journal of veterinary internal medicine · 2026Review
- Genetic and pathway complexity in Alzheimer's disease: Insights from multi-omic data about the immune response and mitochondrial function.Neural regeneration research · 2026Article
- Single-cell RNA sequencing and spatial transcriptomics in the discovery of kidney disease potential biomarkers: a narrative review.BMC nephrology · 2026Review
- Proximal TGF-β Signaling in Chronic Injury: from a notorious fibrotic factor to a repair ally.Pflugers Archiv : European journal of physiology · 2026Review
- Cellular microenvironment of erythropoietin-producing cells in hypoxic and injured mouse kidneys.Experimental physiology · 2026Article
- Hepatocyte growth factor blocks epithelial-mesenchymal transition and fibrosis of ureteral epithelial cells in UPJO.BMC pediatrics · 2026Article
- The Interaction Between Mitophagy Dysregulation and the Diabetic Bladder Microenvironment.Journal of diabetes · 2026Review
- Nanotechnology-Driven Precision Modulation of Transplant Immunity: From Mechanistic Insights to Clinical Tolerance.International journal of nanomedicine · 2026Review
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- MAGL-18c attenuates LPS-induced sepsis-associated liver injury by inhibiting TGF-β/Smad signaling and remodeling medium- and long-chain fatty acid metabolism.Frontiers in immunology · 2026Article
- Affinity-Based Protein Profiling Revealed that HIGD1A is a Direct Target Protein of Aristolochic Acids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- Bioinformatics reveals TNFAIP6 as a candidate gene and suggests its potential crosstalk in the treatment of hemodialysis in chronic kidney disease.Renal failure · 2025Article
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- A New Strategy for Treating Renal Fibrosis Based on a Drug-Food Homogeneous Formula of Traditional Chinese Medicine.Food science & nutrition · 2025Article
- Lysosome stress response and mitochondria injury are the earliest detectable alteration in FSGS.Scientific reports · 2025Article
- MARY1 restores mitochondrial homeostasis and accelerates renal recovery following acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Asprosin Aggravates Tubular Epithelial Cell Injury and Phenotypic Transformation via Mitochondrial Dynamics Disorder Mediated by Excessive Drp1 SUMOylation in Diabetic Nephropathy Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
Abstract
Excessive TGF-β signaling and mitochondrial dysfunction fuel chronic kidney disease (CKD) progression. However, inhibiting TGF-β failed to impede CKD in humans. The proximal tubule (PT), the most vulnerable renal segment, is packed with giant mitochondria and injured PT is pivotal in CKD progression. How TGF-β signaling affects PT mitochondria in CKD remained unknown. Here, we combine spatial transcriptomics and bulk RNAseq with biochemical analyses to depict the role of TGF-β signaling on PT mitochondrial homeostasis and tubulo-interstitial interactions in CKD. Male mice carrying specific deletion of Tgfbr2 in the PT have increased mitochondrial injury and exacerbated Th1 immune response in the aristolochic acid model of CKD, partly, through impaired complex I expression and mitochondrial quality control associated with a metabolic rewiring toward aerobic glycolysis in the PT cells. Injured S3T2 PT cells are identified as the main mediators of the maladaptive macrophage/dendritic cell activation in the absence of Tgfbr2. snRNAseq database analyses confirm decreased TGF-β receptors and a metabolic deregulation in the PT of CKD patients. This study describes the role of TGF-β signaling in PT mitochondrial homeostasis and inflammation in CKD, suggesting potential therapeutic targets that might be used to mitigate CKD progression.
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