Ask about this productRelated genes to: LPCAT1 Blocking Peptide
- Gene:
- LPCAT1 NIH gene
- Name:
- lysophosphatidylcholine acyltransferase 1
- Previous symbol:
- AYTL2
- Synonyms:
- FLJ12443, AGPAT9, AGPAT10
- Chromosome:
- 5p15.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-03
- Date modifiied:
- 2015-08-26
Related products to: LPCAT1 Blocking Peptide
Related articles to: LPCAT1 Blocking Peptide
- Late-onset silicosis is characterized by the progression of pulmonary fibrosis long after cessation of silica exposure, yet its underlying mechanisms remain poorly understood. This study aimed to determine whether a brief silica exposure could initiate a sustaining fibrotic process and to characterize the associated pathological and molecular alterations. A rat model of silicosis was established by short-term silica inhalation for two weeks, followed by a recovery period of up to 46 weeks. Histopathological and micro-CT analyses demonstrated progressive fibrotic development even after exposure cessation. Notably, fibrotic pulmonary dust foci (fPDFs) emerged as a predominant lesion, characterized by alveolar remodeling and diffuse collagen deposition distinct from classical silicotic nodules. These lesions were associated with alveolar type II (AT2) cell dysfunction, evidenced by aberrant differentiation, loss of homeostatic markers such as ATP-binding cassette subfamily A member 3 (ABCA3), lysophosphatidylcholine acyltransferase 1 (LPCAT1), and fatty acid synthase (FAS), and gain of transitional markers keratin 8 (KRT8) and stratifin (SFN). Integrated proteomic and lipidomic analyses revealed profound metabolic reprogramming, with significant dysregulation of lipid metabolism pathways. Key enzymes involved in lipid synthesis and remodeling were identified in AT2 cells and downregulated in fPDF regions. Our findings establish that short-term silica exposure initiates a sustaining fibrotic cascade, highlight fPDFs as a critical pathological entity, and suggest that AT2 cell dysfunction and metabolic reprogramming are closely associated with the progression of silicosis, highlighting them as potential key correlates of the sustaining fibrotic cascade. These insights provide a novel framework for understanding disease progression and identifying therapeutic targets. - Source: PubMed
Publication date: 2026/05/20
Yang XinyueHai YinongChen YuqiXu DingjieLi YaqianJin FuyuWei ZhongqiuZhu YingGao XueminCai WenchenLi TianMao NaXu Hong - Lung cancer is the leading cause of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for 80-85% of cases. Cisplatin (DDP) is a first-line chemotherapy drug for NSCLC, but acquired DDP resistance severely limits therapeutic efficacy. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is involved in tumor progression, but its role in DDP resistance of NSCLC remains unclear. This study aimed to investigate the regulatory mechanism of LPCAT1 in DDP-resistant NSCLC and explore the potential role of tripartite motif-containing 33 (TRIM33) in modulating LPCAT1. - Source: PubMed
Publication date: 2026/05/08
Huang JieWang Bao QingWu QinWang Li MingGuan Chao - Lactate has been proven to be an important metabolite involved in tumor initiation, progression, and tumor microenvironment, affecting patient prognosis. The role of lactate metabolism-related genes in liver cancer is unclear. - Source: PubMed
Publication date: 2026/05/13
Li DingLi MuziYan MengfanXiong Yuanyuan - Given the lack of effective targeted therapeutic options for triple-negative breast cancer (TNBC), there is an imperative demand for innovative treatment approaches, with ferroptosis standing out as a promising direction. This study identifies HSPA6 as a key ferroptosis sensitizer in TNBC. Mechanistically, HSPA6 binds to NF-κB p65, inhibits its nuclear translocation and Ser468 phosphorylation, thereby suppressing transcription of the lipogenic enzyme FASN and downregulating phospholipid-remodeling enzymes LPCAT1/cPLA2. This dual inhibition enriches membrane phospholipids with polyunsaturated fatty acids, heightening peroxidation susceptibility and triggering ferroptosis. Concurrently, HSPA6-mediated suppression of lipogenesis depletes palmitate, thereby attenuating ANKIB1 palmitoylation and inhibiting its E3 ligase activity. This impairs K48-linked ubiquitination and degradation of HSPA6, forming a stabilizing positive feedback loop. Our study uncovers a HSPA6-p65-FASN-ANKIB1 axis linking lipid metabolism to ferroptosis, offering a novel TNBC therapeutic target. - Source: PubMed
Publication date: 2026/04/08
Hai Lin-YueYu Zhi-HaoLiu Wen-BoZhang Yuan-YuanXu YueCheng ShanYue Hao-RanGuo Zhang-YinYan Shi-JieSun RuiLiu Xiao-FengLiu Bo-WenWang XinCao Xu-ChenYu Yue - - Source: PubMed
Publication date: 2026/04/15
Jiang LipingXu SumeiPeng JingboYu JingWu HuilanWu WeiHuang ZhichunPan JieTan Zhirong