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October 5, 2025Open Access

Trem2+ macrophages alleviate renal tubule lipid accumulation and ferroptosis in Diabetic Nephropathy by repressing IL-1β-mediated CD36 expression

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Authors

XWXue WangJWJiayi WanCWChao Wang

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Overview

Experimental analysis reveals Trem2+ macrophages reduce lipid accumulation and IL-1β-induced ferroptosis in diabetic nephropathy, suggesting a protective mechanism.

Key Points

  • Trem2+ macrophages effectively reduce lipid accumulation and prevent ferroptosis in tubular cells during diabetic nephropathy.
  • Key evidence shows that Trem2-deficient macrophages increase il-1β production, promoting harmful CD36 expression.
  • Observational analysis in diabetic mouse models highlights Trem2's protective role and its effect on the renal microenvironment.
  • These findings underscore the potential for targeting trem2+ macrophages in therapeutic approaches for diabetic nephropathy.

Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/68e24e6bd6d66a53c2473ac3https://doi.org/10.2337/figshare.29954540
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Trem2+ Macrophages Alleviate Renal Tubule Lipid Accumulation and Ferroptosis in Diabetic Nephropathy by Repressing IL-1β–Mediated CD36 Expression2025 · 13 citations
  2. 2Targeting Myeloid Trem2 Reprograms the Immunosuppressive Niche and Potentiates Checkpoint Immunotherapy in NASH-Driven Hepatocarcinogenesis2025 · 16 citations
  3. 3Data from Targeting Myeloid Trem2 Reprograms the Immunosuppressive Niche and Potentiates Checkpoint Immunotherapy in NASH-Driven Hepatocarcinogenesis2025
  4. 4Mechanisms by which macrophage Ltb4r1 mediates tubular epithelial cell injury to facilitate the advancement of diabetic kidney disease2026
  5. 5Trem2 regulates macrophage phenotype via the JAK2/STAT3 signaling pathway to ameliorate ventricular remodeling after acute myocardial infarction2026