
Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 16, 2024
Language: Английский
Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 16, 2024
Language: Английский
Immunity, Journal Year: 2024, Volume and Issue: 57(9), P. 2122 - 2139.e9
Published: Aug. 28, 2024
Language: Английский
Citations
22Proceedings of the National Academy of Sciences, Journal Year: 2024, Volume and Issue: 121(8)
Published: Feb. 15, 2024
Coordinated metabolic reprogramming and epigenetic remodeling are critical for modulating T cell function differentiation. However, how the modification controls Th17/Treg balance via remains obscure. Here, we find that Setd2, a histone H3K36 trimethyltransferase, suppresses Th17 development but promotes iTreg polarization phospholipid remodeling. Mechanistically, Setd2 up-regulates transcriptional expression of lysophosphatidylcholine acyltransferase 4 (Lpcat4) directly catalyzing H3K36me3
Language: Английский
Citations
7Clinical Reviews in Allergy & Immunology, Journal Year: 2025, Volume and Issue: 68(1)
Published: Jan. 27, 2025
Language: Английский
Citations
0Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)
Published: March 28, 2025
Abstract Abnormal metabolic reprogramming is essential for tumorigenesis, metastasis, and the regulation of immune responses. Fatty acid synthase (FASN), a key enzyme in lipid metabolism, plays crucial role these processes. However, relationship between FASN-mediated response colorectal cancer (CRC) remains unclear. The present study demonstrated that FASN expression elevated CRC tissues significantly associated with poor prognosis. Functional experiments revealed promotes proliferation, migration, invasion, phosphatidylcholine (PC) production cells. Additionally, vivo knockdown inhibits tumor growth spread cells to lungs. Mechanistically, FASN, which upregulated tissues, drives cell PC metabolism through SP1/PLA2G4B axis, subsequently suppressing antitumor natural killer (NK) PC-dependent manner. These findings provide new insights into immunobiology CRC, suggesting potential targets treatment prevention CRC.
Language: Английский
Citations
0Genes & Diseases, Journal Year: 2025, Volume and Issue: unknown, P. 101622 - 101622
Published: April 1, 2025
Language: Английский
Citations
0Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15
Published: Sept. 30, 2024
Background Pancreatitis is a serious and complex inflammatory disease that imposes severe effect on quality of life. Links between plasma lipidome pancreatitis have been reported, some which not yet clearly elucidated. Methods Therefore, our study aimed to investigate the causal relationships four types by conducting bidirectional, two-sample Mendelian randomization (MR) analysis. We obtained genetic variants associated with 179 lipid species from Genome-wide association analysis lipidome. The aggregated statistical data acute (AP), alcohol-induced (AAP), chronic (CP), (ACP) FinnGen consortium were exploited as outcome. inverse variance weighted (IVW) technique main method was used for MR sensitivity analyses evaluate heterogeneity pleiotropy. Results After FDR correction, SE (27:1/20:4) (OR = 0.938, 95%CI 0.906-0.972, P 4.38 × 10 -4 , PFDR 0.039) identified be significantly AP risk. Eight CP risk: 0.911, 0.869-0.954, 8.89 -5 0.016), LPC (20:4) 0.892, 0.843-0.945, 9.74 0.009), PC (16:0_22:5) 0.880, 0.818-0.947, 6.29 0.028), (17:0_20:4) 0.893, 0.842-0.948, 1.76 0.010), (18:0_20:4) 0.920, 0.874-0.969, 1.70 -3 0.038), (O-16:0/20:4) 0.871, 0.804-0.943, 6.95 0.025), (O-16:1/20:4) 0.890, 0.832-0.953, 7.85 0.023), PE (O-18:1/20:4) 0.866, 0.791-0.947, 1.61 0.041). Furthermore, genetically predicted increased 0.862, 0.796-0.934, 3.00 0.027) SM (34:2;O2) 0.753, 0.659-0.860, 2.97 0.005) levels decreased risk ACP. Conclusions Our findings provide evidence associations specific pancreatitis, offering new insights into future clinical research.
Language: Английский
Citations
2Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 16, 2024
Language: Английский
Citations
0