ReviewOncology reviews2026
Lipid metabolic reprogramming in clear cell renal cell carcinoma: focus on high-density lipoprotein-related pathways.
Review in Oncology reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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0 citing papers in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clear cell renal cell carcinoma (ccRCC) is one of the most prevalent solid tumors characterized by lipid metabolic reprogramming, with extensive lipid droplet accumulation in tumor cells as a hallmark feature. Traditionally, this phenotypic trait is attributed to enhanced fatty acid synthesis, increased triglyceride (TG) storage, and impaired β-oxidation. However, emerging transcriptomic and lipidomic evidence suggests that cholesterol metabolism is also profoundly reprogrammed in ccRCC, particularly via increased reliance on high-density lipoprotein (HDL)-derived cholesterol. The classical fatty acid-TG pathway and the HDL-cholesterol axis are metabolically linked through shared substrates, collectively shaping lipid homeostasis in ccRCC. In this review, we summarize recent advances in ccRCC lipid metabolic reprogramming, with a focus on HDL-related cholesterol metabolism. We discuss the mechanisms involving von Hippel-Lindau (VHL) loss and hypoxia-inducible factor (HIF) activation, including SCARB1-mediated cholesterol uptake, LXRα-ABCA1/ABCG1-dependent cholesterol efflux, and SOAT1-driven re-esterification of free cholesterol into cholesteryl esters (CE). Furthermore, we outline potential therapeutic targets within these pathways and highlight critical knowledge gaps that merit further investigation. This review provides a conceptual framework for understanding HDL-centered cholesterol metabolism in ccRCC and highlights potential metabolic vulnerabilities for therapeutic targeting.
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Registered trials
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