Ask about this productRelated genes to: PAI1 antibody
- Gene:
- SERPINE1 NIH gene
- Name:
- serpin family E member 1
- Previous symbol:
- PLANH1, PAI1
- Synonyms:
- PAI
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: PAI1 antibody
Related articles to: PAI1 antibody
- Crystalline nephropathy is driven by a self-perpetuating cycle in which crystal-induced tubular injury promotes further nucleation, growth, and aggregation, transforming the kidney into a pathological mineralization niche. Conventional therapies fail to disrupt this vicious loop, while nanomedicines are hindered by the glomerular filtration barrier (<10 nm), and natural antioxidants like protocatechuic acid (PCA) suffer from poor bioavailability. Here, we report a 7.3 nm mitochondria-targeted metal-polyphenol network (Fe-PCA@TPP) that overcomes both delivery and targeting challenges to directly intervene at sites of redox imbalance. Formed via PCA-Fe coordination and functionalized with triphenylphosphonium (TPP), Fe-PCA@TPP efficiently traverses the glomerular barrier, accumulates selectively in mitochondria, scavenges free radicals broadly, restores redox homeostasis, and potently inhibits calcium oxalate (CaOx) crystal nucleation, growth, and aggregation. In vitro, Fe-PCA@TPP protects renal tubular epithelial cells from oxalate-induced oxidative stress by preserving mitochondrial bioenergetics and preventing apoptosis. In vivo, it preferentially accumulates in the kidney, reduces CaOx deposition, improves renal function, and downregulates markers of injury and inflammation. Mechanistically, Fe-PCA@TPP targets Plasminogen Activator Inhibitor Type 1 (SerpinE1) to block oxidative stress-apoptosis cascades, thereby remodeling the intrarenal pathological microenvironment. This work presents a size-compatible, mitochondria-targeted, and SerpinE1-specific nanoplatform that integrates crystal inhibition, redox regulation, and efficient renal clearance, offering a promising therapeutic strategy for crystalline nephropathy. - Source: PubMed
Publication date: 2026/05/14
Chen Xue-WuLong JunZheng Xiao-PengYu Bang-XianWang Guang-ZhaoWu Wen-QiLiu Yong-DaZeng Guo-HuaHuang Ling-HongSun Xin-Yuan - Mounting evidence points to a potential link between statin therapy and erectile dysfunction (ED). However, the underlying mechanisms remain elusive, particularly concerning potential statin disruption of the inflammatory and immunofibrotic microenvironment within erectile tissue. This study sought to elucidate statin-associated ED and identify key molecular and cellular mediators driving this process. - Source: PubMed
Publication date: 2026/03/24
Zhang YangWen SongZhu YanpingZhang QinyongZheng PengyiWang XiaohuiLv Shuangwu - Hepatocellular carcinoma (HCC) is the predominant type of primary liver cancer. This study aimed to elucidate the involvement of genes associated with 25 cell-death modalities in HCC development and progression. HCC transcriptomic datasets were integrated with curated cell death-related genes. Candidate genes were screened by differential expression analysis and protein-protein interaction network construction. Prognostic genes were identified using univariate Cox regression, proportional hazards assumption testing, and stepwise multivariate Cox regression. A risk score model and a nomogram were established, followed by risk stratification and analyses of immune infiltration, immune checkpoints, somatic mutations, and in silico drug sensitivity. Single-cell RNA sequencing was used to identify key cell types, infer temporal dynamics, and characterize intercellular communication, and findings were validated by quantitative real-time PCR (qRT-PCR). MAPT, CDKN2A, NQO1, CHGA, SERPINE1, and RET were identified as prognostic genes, and the risk model and nomogram showed good prognostic performance. Immune profiling revealed significant differences in multiple immune cell subsets between risk groups, including activated CD4+ T cells. Notably, CDKN2A correlated with activated CD4+ T cells, NQO1 with natural killer cells, RET with CD4+ central memory cells, and SERPINE1 with activated dendritic cells; RET also showed the strongest positive correlation with HAVCR2. Mutation spectra differed across risk groups, and ten drugs displayed significant predicted IC50 differences; all six genes were negatively correlated with KIN001.135. Single-cell analyses highlighted hepatocytes as a key cell type with strong hepatocyte-epithelial communication. qRT-PCR confirmed higher MAPT, CDKN2A, NQO1, and SERPINE1 expression in HCC tissues than in normal tissues. - Source: PubMed
Publication date: 2026/04/22
Wu WeiWang YingjiZhao XiaochengDong KeLi MaodeAn XiangXu YingyanWang ShuaiLi Dexin - This integrated multi-omics study delineates molecular alterations in the substantia nigra pars compacta (SNpC) across different stages of Parkinson's disease (PD) in a Korean cohort. By combining transcriptomic and proteomic analyses of postmortem tissues, we identified stage-specific molecular signatures associated with Braak Lewy body pathology. Enrichment analyses revealed upregulation of extracellular matrix-related and immune response pathways, along with downregulation of genes involved in microtubule organization and neuronal function in the SNpC of PD patients. In addition, fifteen genes and fourteen proteins showing significant fold changes (>2.0 or <0.5), high normalized expression levels (log2 >3.0) and statistical significance (p<0.05) were profiled. Hierarchical clustering and principal component analysis of transcriptomic and proteomic data from SNpC tissues of PD patients (selected based on correlation coefficients >0.8 or <-0.8) revealed distinct stage-dependent groupings aligned with Braak Lewy body pathology. Molecular profiles correlated strongly with disease progression; advanced Braak stages exhibited disrupted mitochondrial processes and elevated phospholipid binding pathways, potentially linked to α-synuclein aggregation and neurodegeneration. Notably, upregulation of genes such as and was associated with α-synuclein aggregation, cell death, and autophagy inhibition, while downregulation of , and co-occurred with neuronal loss and mitochondrial dysfunction. Proteomic analyses further highlighted increased levels of neuroinflammation and mitochondrial impairment markers, including SNCA, GPNMB, and LGALS3, some of which may serve as biomarkers of disease severity. These findings offer critical insights into PD's molecular pathogenesis and identify potential candidates for further functional validation and therapeutic intervention. - Source: PubMed
Publication date: 2026/05/14
Kim SinyeonChoi Jin GyuKim Se WoongSon MiwonKim DaehwanNam Soo JeongKim Sang JinKim Seongheon - High-grade soft tissue sarcomas (STSs) are heterogeneous tumours lacking robust prognostic or predictive biomarkers. Regnase-1, an immune RNase, enhances antitumour immunity by limiting immunosuppressive tumour microenvironment (TME) components (e.g., myeloid-derived suppressor cells (MDSCs)), but remains unexplored in STS. As CD68 tumour-associated macrophages (TAMs) drive TME suppression and poor prognosis in non-translocation-driven STS, we evaluated Regnase-1 and CD68 TAMs to assess Regnase-1 as an indicator of an immunologically activated TME. - Source: PubMed
Publication date: 2026/04/29
Zangarini JulieKünstner AxelLenz FlorianTharun LarsVorwerk JanGebauer NiklasKirfel JuttaBusch HaukeKöhler Bruno ChristianWardelmann EvaRades DirkLöser AnastassiaBubnoff Nikolas vonKhandanpour CyrusKebenko Maxim