HMGCS2 (3-Hydroxy-3-Methylglutaryl-CoA Synthase 2)

This study comprehensively characterized the molecular features of ArMGs in GC and developed a robust, validated prognostic prediction model. The findings offer new molecular insights for predicting patient outcomes and guiding personalized therapeutic strategies in GC.

Single-cell analysis identified six major cell types, providing a deeper understanding of the cellular heterogeneity within LIHC. In summarize, this study presents the first integrated apoptosis-cholesterol metabolic pathway-based six-gene prognostic model for LIHC, validated for robustness across multiple cohorts, which may facilitate personalized therapeutic strategies and refined risk assessment in clinical practice.

Across subcutaneous and orthotopic models, combined treatment with carotuximab and irradiation reproducibly achieved superior tumor volume reduction relative to single-agent therapy. This study identified the BMP/CD105 axis as a key pathway in radiation resistance, highlighting the potential of targeting fibroblastic CD105 with carotuximab to enhance radiation sensitivity.

In addition, XFC partially reversed the effects of the PPARγ antagonist GW9662, activated the PPARγ signaling pathway, inhibited oxidative stress and inflammatory responses, and exerted anti-fibrotic effects similar to those of the PPARγ agonist rosiglitazone. XFC inhibits inflammation and oxidative stress by regulating the PPARγ/HMGCS2 pathway, thereby attenuating fibrosis and alleviating lung injury.

In summary, we have identified a novel role for C3G in the liver as a key mediator of hepatocyte differentiation and metabolic functions of hepatocytes. Hence, its absence leads to an immature phenotype and an altered response to insulin and glucagon, favoring glucagon actions.

This study highlights the diagnostic and prognostic significance of ACSM3 and describes the METTL14/ACSM3/GATA5/ HMGCS2/mTORC1 axis in a comprehensive study of ccRCC. These results provide a solid basis for research on ccRCC to explore new diagnostic and treatment strategies.

Mechanistically, cynaroside exerted therapeutic effects via HMGCS2-mediated ketogenesis. Our data demonstrated that ketogenic modulation is a viable therapeutic strategy to delay T2DM-NAFLD progression.

The lower part of the figure highlights that succinylation promotes tumor cell hypoxic adaptation and immune escape by stabilizing HIF-1α, inducing ROS production, and SDH dysfunction. TCA, Tricarboxylic acid cycle PDH, Pyruvate dehydrogenase SDH, Succinate dehydrogenase GLUD1, Glutamate dehydrogenase 1 HMGCS2, 3-hydroxy-3-methylglutaryl-CoA synthase 2 FEN1, Flap endonuclease 1, SIRT, Sirtuin family proteins, KAT2A, Lysine acetyltransferase 2A alpha-KGDH, Alpha-ketoglutarate dehydrogenase CPT1A, Carnitine palmitoyltransferase 1A HAT1, Histone acetyltransferase 1 HIF-1α, Hypoxia-inducible factor 1 alpha ROS Reactive oxygen species.This figure was created by Biorender.com.(https://BioRender.com).

Cholesterol metabolism-related features are a promising biomarker for predicting THCA prognosis and can potentially guide personalized immunization and targeted therapy.

Molecular hydrogen confers protection against cisplatin-induced nephrotoxicity by modulating β-HOB metabolism through upregulation of HMGCS2, thereby suppressing renal inflammation and apoptosis. These findings provide new insights into the metabolic mechanism underlying H2's tissue-protective effects and offer a theoretical foundation for its potential clinical application in mitigating chemotherapy-induced kidney injury.

Therapeutically, Esr2 agonists restored kidney function in Mfap2-deficient models. These findings position Mfap2 as a key regulator of ECM dynamics and mechanosignaling, linking tissue stiffness to metabolic reprogramming required for kidney repair.

Combined with protein profiling data, we speculate that SNHG11 may be involved in osteosarcoma progression by binding to SERPINB12 and regulating transcription. In conclusion, lncRNA SNHG11 plays a critical role in osteosarcoma development by regulating cellular information carriers at the DNA, RNA, and protein levels.