Ask about this productRelated genes to: ACADL Blocking Peptide
- Gene:
- ACADL NIH gene
- Name:
- acyl-CoA dehydrogenase long chain
- Previous symbol:
- -
- Synonyms:
- LCAD, ACAD4
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1988-11-07
- Date modifiied:
- 2017-09-21
Related products to: ACADL Blocking Peptide
Related articles to: ACADL Blocking Peptide
- Aberrant epithelial remodeling, driven by a shift from ciliated to goblet cell ratio, is central to chronic nasal inflammation. Despite the known role of metabolism in normal epithelial differentiation, the specific metabolic reprogramming patterns underlying this pathological shift of nasal epithelium induced by type 2 inflammatory milieu is poorly understood. This study aimed to delineate the key metabolic pathways involved in aberrant nasal epithelial differentiation. - Source: PubMed
Publication date: 2026/04/27
Lin YutongYe XiaoyanZhong YingqianLi LiyueHuang XianxiongChen HexinMeng QingxiangGao YifangLi JianHuang JianfengLi Chunwei - Metabolic dysfunction-associated fatty liver disease (MAFLD) remains a global health burden with limited definitive therapies, highlighting the need for safe, food-derived interventions. Salvianolic acid B (SALB), a major water-soluble bioactive component of the traditional Asian health-promoting food , exhibits lipid-lowering, anti-inflammatory, and antioxidant properties, but its therapeutic potential and mechanisms in MAFLD remain unclear. Here, we employed an integrated approach combining network pharmacology, molecular docking, surface plasmon resonance affinity assays, lipidomics, and experiments in vitro and in vivo to address this gap. Network pharmacology combined with lipidomics identified PPAR-α as a key target of SALB. Molecular docking and SPR assays confirmed direct binding between SALB and PPAR-α. In vitro, SALB reduced triglyceride levels and lipid accumulation in HepG2 cells, enhanced fatty acid oxidation (FAO), and upregulated PPAR-α, PGC-1α, and FAO-related genes (CPT1, CPT2, ACADL, ACADVL). In HFD-fed mice, SALB decreased serum total cholesterol, triglycerides, LDL-C, ALT, AST, while increasing HDL-C. Additionally, SALB upregulated hepatic PPAR-α and FAO-related gene expression and suppressed hepatic reactive oxygen species production and inflammatory responses in both models. Collectively, our findings demonstrate that SALB, a natural food-derived bioactive compound, targets PPAR-α to ameliorate MAFLD by enhancing FAO, modulating lipid metabolism, and mitigating oxidative stress and inflammation. This work supports SALB's potential as a dietary supplement for MAFLD and metabolic disease management, reinforcing the value of exploring functional components from health-promoting food. - Source: PubMed
Publication date: 2026/03/19
Huang FengyanQiu ChenWang DannaNi YuanyingFu ZhuotaoFu LinchunLiang ChaoHuang ShangyiDeng Zhitong - Colon cancer (CC), a malignancy with high global incidence and mortality, remains a major public health burden. As a pivotal aspect of tumor metabolic reprogramming, fatty acid metabolism has drawn significant research interest. This study was designed to elucidate the relationship between fatty acid metabolism-related gene expression and prognosis in patients with CC. - Source: PubMed
Publication date: 2026/03/15
Zhou ShulingChen MinDong ZhikunYang YongShi XiaoruiKang HuanShi ChangbeiWang Xuan - Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid-laden macrophage foam cell formation and defective efferocytosis. This study aims to investigate the impact of GFPT2 on macrophage function in AS and its underlying mechanisms. - Source: PubMed
Publication date: 2026/04/14
Ke KunYan LeyeChen RongZhang ChuanrongYang WeizhuZhang ZefuLin Junqing - Fatty liver hemorrhagic syndrome (FLHS) is a nutrition-related metabolic disorder in laying hens characterized by excessive hepatic lipid accumulation and hemorrhagic lesions, leading to reduced productivity and increased mortality. However, the regulatory mechanisms linking mitochondrial dysfunction to hepatic lipid metabolism remain unclear. This study investigated the role of SIRT3 in modulating mitochondrial fatty acid oxidation during FLHS progression. An in vivo FLHS model was established by feeding laying hens with a high-energy, low-protein (HELP) diet, and an in vitro hepatic steatosis model was induced by free fatty acid (FFA) treatment in primary hepatocytes. Both models exhibited pronounced lipid accumulation in hepatic cells and altered hepatocellular injury-related parameters, which were associated with mitochondrial dysfunction and impaired fatty acid oxidation. Mechanistically, hepatic tissues and hepatocytes showed suppression of the SIRT3-AMPKα-PGC-1α signaling cascade, accompanied by reduced expression of mitochondrial biogenesis markers (NRF1, TFAM), impaired respiratory chain components (NDUFA9, SDHA, UQCRC1, COX4I1, ATP5B), and decreased transcription of fatty acid oxidation-related genes (PPARα, ACOX1, CPT1A, CPT2, ACADL, ACADM). Pharmacological activation of SIRT3 with AR-C17 restored AMPKα-PGC-1α signaling, enhanced mitochondrial biogenesis and respiratory function, and promoted fatty acid oxidation, thereby alleviating lipid accumulation in hepatocytes in both models. Collectively, these results demonstrate that SIRT3 is a key metabolic regulator maintaining mitochondrial oxidative function and lipid homeostasis in laying hens. Targeted activation of SIRT3 may provide a novel nutritional strategy for preventing or ameliorating FLHS and related metabolic disturbances in poultry production. - Source: PubMed
Publication date: 2026/04/07
Cao PanpanChen JinyanZeng ChunHu YangYuan JianyunGuo XiaoquanCao HuabinZhang CaiyingZhuang YuHu Guoliang