Ask about this productRelated genes to: COL3A1 protein
- Gene:
- COL3A1 NIH gene
- Name:
- collagen type III alpha 1 chain
- Previous symbol:
- EDS4A
- Synonyms:
- -
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: COL3A1 protein
Related articles to: COL3A1 protein
- Whether spontaneous cervical artery dissection (sCeAD), the leading cause of ischemic stroke in young adults, represents the manifestation of unrecognized hereditary connective tissue disorders (HCTDs) and whether HCTDs have a major impact in the epidemiology of the disease is a matter of ongoing debate. We aimed at determining the frequency of clinically relevant genetic variants (CRGVs) in a cohort of unselected sCeAD patients by targeted next-generation sequencing (NGS) approach. - Source: PubMed
Publication date: 2026/09/02
Corradi LorenzoFerraro ChiaraTesi FiammettaAbrignani GiorgiaCastellini PaolaLatte LiliaTrapasso Maria ClaudiaGenovese AntonioRitelli Marco GiuseppeCinquina ValeriaGiliani Silvia ClaraMagoni MauroMenozzi RobertoPezzini Alessandro - This study aimed to investigate the imaging characteristics and molecular mechanisms by which pelvic floor electrical stimulation (PFES) improves pelvic floor muscle injury in a rat model of stress urinary incontinence (SUI). - Source: PubMed
Publication date: 2026/09/01
Li ChenWang ZiyuYue GuangDeng HanLiao LiminJin LinquanLi Xing - Spontaneous coronary artery dissection (SCAD) is characterized by a separation of the coronary artery wall, causing myocardial infarction and sudden death. This study is one of the first to clarify the impact of pathological genetic variants in candidate SCAD-related genes on the histopathological and morphological properties of human SCAD lesions. - Source: PubMed
Publication date: 2026/09/01
Tanaka TakamasaKawakami RikaGaynor Brady JWilliams DesireeAugenstreich JacquesSakamoto AtsushiJinnouchi HiroyukiKawai KenjiKonishi TakaoShiraki TatsuyaSekimoto TeruoNakayama TakafumiFujiyoshi KazuhiroHamana TomoyoAdachi YusukeDiaz Keisha MedinaHong Charles CGrogan AlyssaMitchell Braxton DVirmani RenuFinn Aloke V - Activated hepatic stellate cells (HSCs) play a central role in liver fibrosis by promoting extracellular matrix deposition, oxidative stress, and pro-fibrotic signaling. Here, we engineered a membrane-fused hybrid nanoparticle by combining grape-derived exosome-like particles (GELPs) with liposomes to encapsulate JQ1, termed Hybrid@JQ1, and evaluated its anti-fibrotic effects in TGF-β1-activated LX-2 cells. GELPs were successfully isolated and characterized, while the formation of GELP-liposome hybrid nanoparticles were verified by nanoparticle characterization and colocalization analysis. Hybrid@JQ1 exhibited good physicochemical stability and enhanced cellular uptake. In vitro, Hybrid@JQ1 inhibited LX-2 cell proliferation and migration, decreased collagen accumulation, and suppressed α-SMA expression. qPCR gene expression profile further showed that Hybrid@JQ1 downregulated multiple fibrosis-related genes, including α-SMA, COL1A1, COL3A1, and TGF-β, as well as inflammation- and oxidative stress-associated genes such as NOX4, IL6, and TNF-α. These findings indicate that GELP-liposome hybridization is an effective strategy for JQ1 delivery and that Hybrid@JQ1 alleviates fibrotic phenotypes in activated HSCs in vitro. Our study provides a promising plant-derived biomimetic nanoplatform for anti-fibrotic drug delivery. - Source: PubMed
Publication date: 2026/08/29
Han XiaoxueLu RongtingZhang YijiaBushra AnikaIrudayaraj Joseph - Neutrophils exert diverse functions in parasitic infections, including pathogen clearance and regulation of inflammation. However, their specific roles in the early stage of infection with (), a significant foodborne parasite that dwells in the bile ducts, remain largely unknown. In this study, FVB mice were orally infected with 50 metacercariae, and neutrophils were depleted using an anti-Ly6G antibody whereas IgG isotype served as the control. Mice were sacrificed 14 days post-infection, and serum and liver tissue were collected to assess hepatobiliary injury. Hepatic leukocyte changes were analyzed by flow cytometry, and associated cytokine/chemokine expression was detected by qPCR. Results showed that neutrophil-depleted mice exhibited significantly aggravated hepatobiliary injury, as evidenced by elevated serum ALT/AST, epithelial hyperplasia, inflammatory infiltration, and ductal dilatation. Neutrophil depletion also exacerbated infection-induced hepatic fibrosis, indicated by increased collagen fiber deposition and increased mRNA levels of , and . Flow cytometry revealed reduced absolute T cell counts but increased CD45CD11bF4/80 Kupffer cells and CD45CD11bLy6GLy6C monocytes in neutrophil-depleted infected mice. Additionally, neutrophil depletion increased mRNA levels of , , , , , , , and , while down-regulating in infected mice. Collectively, these findings indicate a protective role of neutrophils in the early infection in this murine model. Neutrophil depletion induces compensatory expansion of Kupffer cells and Ly6C monocytes, forming a pro-inflammatory and pro-fibrotic microenvironment that accelerates liver damage. The results highlight neutrophils as important modulators of hepatic immune responses during clonorchiasis and point to the need for further investigation into neutrophils-mediated regulation of helminth-associated liver pathology. - Source: PubMed
Publication date: 2026/08/09
Zhang BoRen XinxinLi JiejieSun JingzeShen YingLiu SihanJi QingqingShang JinmanZhang ChenJiang ZhihuaYu QianZheng KuiyangYan ChaoZhang BeibeiHua Hui