Observational studyFrontiers in immunology2021
Impaired ATG16L-Dependent Autophagy Promotes Renal Interstitial Fibrosis in Chronic Renal Graft Dysfunction Through Inducing EndMT by NF-κB Signal Pathway.
Observational study in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Compensatory Mitophagy via NEDD4/HIF-1α/BNIP3 Pathway Restrains EndMT and Renal Allograft Interstitial Fibrosis Induced by TNFα.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- CAV1 promotes epithelial-to-mesenchymal transition (EMT) and chronic renal allograft interstitial fibrosis by activating the ferroptosis pathway.Frontiers in immunology · 2025Article
- Src inhibition modulates AMBRA1-mediated mitophagy to counteract endothelial-to-mesenchymal transition in renal allograft fibrosis.Cell proliferation · 2024Article
- Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.American journal of physiology. Renal physiology · 2024Review
- Rictor/mTORC2 signalling contributes to renal vascular endothelial-to-mesenchymal transition and renal allograft interstitial fibrosis by regulating BNIP3-mediated mitophagy.Clinical and translational medicine · 2024Article
- Plasma-derived exosomes contributes to endothelial-to-mesenchymal transition in Moyamoya disease.Heliyon · 2024Article
- Article
- Advances in the study of key cells and signaling pathways in renal fibrosis and the interventional role of Chinese medicines.Frontiers in pharmacology · 2024Review
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- Macrophage polarization induces endothelium-to-myofibroblast transition in chronic allograft dysfunction.Renal failure · 2023Article
- Disruption of RCAN1.4 expression mediated by YY1/HDAC2 modulates chronic renal allograft interstitial fibrosis.Cell death discovery · 2023Article
- Endothelial Autophagy Dysregulation in Diabetes.Cells · 2023Review
- Autophagy in acute kidney injury and maladaptive kidney repair.Burns & trauma · 2023Review
- Construction of predictive model of interstitial fibrosis and tubular atrophy after kidney transplantation with machine learning algorithms.Frontiers in genetics · 2023Article
- The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.Frontiers in pharmacology · 2023Review
- Identification and cross-validation of autophagy-related genes in cardioembolic stroke.Frontiers in neurology · 2023Article
- Autophagy and its therapeutic potential in diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Review
- Autophagy and Renal Fibrosis.Aging and disease · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic renal graft dysfunction (CAD) is caused by multiple factors, including glomerular sclerosis, inflammation, interstitial fibrosis and tubular atrophy (IF/TA). However, the most prominent elements of CAD are IF/TA. Our studies have confirmed that endothelial-mesenchymal transition (EndMT) is an important source to allograft IF/TA. The characteristic of EndMT is the loss of endothelial marker and the acquisition of mesenchymal or fibroblastic phenotypes. Autophagy is an intracellular degradation pathway that is regulated by autophagy-related proteins and plays a vital role in many fibrotic conditions. However, whether or not autophagy contributes to fibrosis of renal allograft and how such mechanism occurs still remains unclear. Autophagy related 16 like gene (ATG16L) is a critical autophagy-related gene (ARG) necessary for autophagosome formation. Here, we first analyzed kidney transplant patient tissues from Gene Expression Omnibus (GEO) datasets and 60 transplant patients from our center. Recipients with stable kidney function were defined as non-CAD group and all patients in CAD group were histopathologically diagnosed with CAD. Results showed that ATG16L, as one significant differential ARG, was less expressed in CAD group compared to the non-CAD group. Furthermore, we found there were less autophagosomes and autolysosomes in transplanted kidneys of CAD patients, and downregulation of autophagy is a poor prognostic factor. In vitro, we found out that the knockdown of ATG16L enhanced the process of EndMT in human renal glomerular endothelial cells (HRGECs).
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