ArticlePloS one2019
Macrophage phenotype and its relationship with renal function in human diabetic nephropathy.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 85 citations in OpenAlex.
- M1 macrophage-derived exosomes aggravate diabetic nephropathy by regulating the WTAP/S1PR2 axis.Journal of diabetes investigation · 2026Article
- Identification and regulatory mechanism analysis of macrophage-related key genes in diabetic nephropathy.Diabetology & metabolic syndrome · 2026Article
- Differences and significance of macrophage subtypes and regulatory T lymphocytes in the expression of interstitial fibrosis in diabetic nephropathy at different stages.BMC nephrology · 2026Article
- Shenlian (SL) Decoction Treat Diabetic Nephropathy by Regulating M1 Polarization of Macrophages and Pyroptosis of Renal Tubular Epithelial Cells.Journal of diabetes research · 2026Article
- Relationship between complement and macrophage markers with kidney survival in patients with diabetic nephropathy.Acta diabetologica · 2025Article
- Machine learning based identification of anoikis related gene classification patterns and immunoinfiltration characteristics in diabetic nephropathy.Scientific reports · 2025Article
- Acute hyperglycemia induces podocyte apoptosis by monocyte TNF-α release, a process attenuated by vitamin D and GLP-1 receptor agonists.The Journal of steroid biochemistry and molecular biology · 2025Article
- Sweet regulation - The emerging immunoregulatory roles of hexoses.Journal of advanced research · 2025Review
- Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NADAntioxidants (Basel, Switzerland) · 2025Review
- Cross Talk Between Macrophages and Podocytes in Diabetic Nephropathy: Potential Mechanisms and Novel Therapeutics.Mediators of inflammation · 2025Review
- Protein-bound uremic toxins as therapeutic targets for cardiovascular, kidney, and metabolic disorders.Frontiers in endocrinology · 2025Review
- Unveiling macrophage dynamics and efferocytosis-related targets in diabetic kidney disease: insights from single-cell and bulk RNA-sequencing.Frontiers in immunology · 2025Article
- Integrated bioinformatics analysis and in vivo validation of potential immune-related genes linked to diabetic nephropathy.Heliyon · 2024Article
- Fiery Connections: Macrophage-Mediated Inflammation, the Journey from Obesity to Type 2 Diabetes Mellitus and Diabetic Kidney Disease.Biomedicines · 2024Review
- Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagyWorld journal of diabetes · 2024Article
- Identification of key immune-related genes and potential therapeutic drugs in diabetic nephropathy based on machine learning algorithms.BMC medical genomics · 2024Article
- Tonabersat suppresses priming/activation of the NOD-like receptor protein-3 (NLRP3) inflammasome and decreases renal tubular epithelial-to-macrophage crosstalk in a model of diabetic kidney disease.Cell communication and signaling : CCS · 2024Article
- Protective role for kidney TREM2Cell reports · 2024Article
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- The Role of Immune Cells in DKD: Mechanisms and Targeted Therapies.Journal of inflammation research · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to examine the macrophage phenotype and its relationship to renal function and histological changes in human DN and the effect of TREM-1 on high-glucose-induced macrophage activation. We observed that in renal tissue biopsies, the expression of CD68 and M1 was apparent in the glomeruli and interstitium, while accumulation of M2 and TREM-1 was primarily observed in the interstitium. The numbers of CD68, M1, and M2 macrophages infiltrating in the DN group were increased in a process-dependent manner compared with the control group, and the intensities of the infiltrates were proportional to the rate of subsequent decline in renal function. M1 macrophages were recruited into the kidney at an early stage (I+IIa) of DN. The M1-to-M2 macrophage ratio peaked at this time, whereas M2 macrophages predominated at later time points (III) when the percentage of M1/M2 macrophages was at its lowest level. In an in vitro study, we showed that under high glucose conditions, macrophages began to up-regulate their expression of TREM-1, M1, and marker iNOS and decreased the M2 marker MR. However, the above effects of high-glucose were abolished when TREM-1 expression was inhibited by TREM-1 siRNA. In conclusion, our study demonstrated that there was a positive correlation between the M1/M2 activation state and the progress of DN, and TREM-1 played an important role in high-glucose-induced macrophage phenotype transformation.
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