ArticleJCI insight2021
Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Subcutaneous Daratumumab in Recurrent Posttransplant Focal Segmental Glomerulosclerosis: A Report of 2 Cases.Kidney medicine · 2026Article
- A new brake on podocyte injury: ATOH8 meets TGF-β.American journal of physiology. Renal physiology · 2026Article
- Yishen Tongluo formula ameliorates kidney injury modulating inflammation and apoptosis in streptozotocin-induced diabetic kidney disease mice.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Advances in Focal Segmental Glomerulosclerosis Treatment From the Perspective of the Newest Mechanisms of Podocyte Injury.Drug design, development and therapy · 2025Review
- The Lipid-Oxidative Stress Axis: Novel Therapeutic Targets for Podocytopathy.Journal of inflammation research · 2025Review
- The Effect and Mechanism of Fufang Banbianlian Injection in the Treatment of Mesangial Proliferative Glomerulonephritis.Combinatorial chemistry & high throughput screening · 2025Article
- Review
- Podocyte-Specific Deletion of MCP-1 Fails to Protect against Angiotensin II- or Adriamycin-Induced Glomerular Disease.International journal of molecular sciences · 2024Article
- The immunoregulatory roles of non-haematopoietic cells in the kidney.Nature reviews. Nephrology · 2024Review
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Repurposing drugs for diseases associated with podocyte dysfunction.Kidney international · 2023Review
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- Knockout of the neonatal Fc receptor alters immune complex trafficking and lysosomal function in cultured podocytes.PloS one · 2023Article
- Cell-type-specific molecular characterization of cells from circulation and kidney in IgA nephropathy with nephrotic syndrome.Frontiers in immunology · 2023Article
- VEGF-A controls the expression of its regulator of angiogenic functions, dopamine D2 receptor, on endothelial cells.Journal of cell science · 2022Article
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Decoding the Mechanism behind the Pathogenesis of the Focal Segmental Glomerulosclerosis.Computational and mathematical methods in medicine · 2022Article
- Epigenetic Repression of Chloride Channel Accessory 2 Transcription in Cardiac Fibroblast: Implication in Cardiac Fibrosis.Frontiers in cell and developmental biology · 2021Article
- ANGPTL3 in Podocytes Contributes to the Pathogenesis of Lupus Nephritis by Activating MSR1 in Macrophages.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor Twist1 regulates several processes that could impact kidney disease progression, including epithelial cell differentiation and inflammatory cytokine induction. Podocytes are specialized epithelia that exhibit features of immune cells and could therefore mediate unique effects of Twist1 on glomerular disease. To study Twist1 functions in podocytes during proteinuric kidney disease, we employed a conditional mutant mouse in which Twist1 was selectively ablated in podocytes (Twist1-PKO). Deletion of Twist1 in podocytes augmented proteinuria, podocyte injury, and foot process effacement in glomerular injury models. Twist1 in podocytes constrained renal accumulation of monocytes/macrophages and glomerular expression of CCL2 and the macrophage cytokine TNF-α after injury. Deletion of TNF-α selectively from podocytes had no impact on the progression of proteinuric nephropathy. By contrast, the inhibition of CCL2 abrogated the exaggeration in proteinuria and podocyte injury accruing from podocyte Twist1 deletion. Collectively, Twist1 in podocytes mitigated urine albumin excretion and podocyte injury in proteinuric kidney diseases by limiting CCL2 induction that drove monocyte/macrophage infiltration into injured glomeruli. Myeloid cells, rather than podocytes, further promoted podocyte injury and glomerular disease by secreting TNF-α. These data highlight the capacity of Twist1 in the podocyte to mitigate glomerular injury by curtailing the local myeloid immune response.
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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.