Mouse pre-microRNA Expression Construct mir-210
- Known as:
- Mouse pre-microRNA Expression Construct mir-210
- Catalog number:
- mmir-210-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-210
Related genes to: Mouse pre-microRNA Expression Construct mir-210
- Gene:
- MIR210 NIH gene
- Name:
- microRNA 210
- Previous symbol:
- MIRN210
- Synonyms:
- hsa-mir-210
- Chromosome:
- 11p15.5
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-31
Related products to: Mouse pre-microRNA Expression Construct mir-210
Related articles to: Mouse pre-microRNA Expression Construct mir-210
- Chronic Kidney Disease (CKD) poses a growing global health burden, with increasing prevalence driven by risk factors such as aging, metabolic disorders, and environmental influences. As CKD progresses, it frequently leads to renal fibrosis, a pathological condition characterized by excessive extracellular matrix (ECM) accumulation, fibroblast activation, and progressive loss of kidney function, ultimately resulting in end-stage renal disease (ESRD). Despite advances in CKD management, effective therapies to prevent or reverse renal fibrosis remain limited, underscoring the need for innovative therapeutic strategies. MicroRNAs (miRNAs), small non-coding RNA molecules, have emerged as important post-transcriptional regulators of molecular pathways underlying renal fibrosis. These molecules regulate gene expression and participate in critical processes, including fibroblast activation, ECM remodeling, and inflammation, which collectively contribute to CKD progression. Accordingly, miRNAs are promising biomarkers and therapeutic targets, with urinary and circulating miR-21-5p, miR-192-5p, members of the miR-29 family, miR-126, and miR-210 demonstrating potential clinical relevance. This review examines the role of miRNAs in renal fibrosis and CKD progression, with emphasis on fibroblast activation, partial epithelial-mesenchymal transition (EMT)-associated epithelial plasticity, and ECM deposition. Current evidence indicates that miR-21-5p, miR-433-3p, miR-324-3p, and miR-214-3p generally promote profibrotic or injury-associated signaling, whereas the miR-29 and let-7 families predominantly exert antifibrotic effects. Notably, miR-192-5p and miR-214-3p exhibit context-dependent functions according to renal cell type, disease stage, and molecular target. The review also evaluates miRNA-based therapeutic strategies, including antagomiRs, miRNA mimics, and nanoparticle- and extracellular vesicle-based delivery systems, while addressing persistent challenges related to molecular stability, renal-specific delivery, off-target effects, and clinical translation. Overall, this review advances understanding of miRNA-mediated regulation in CKD and highlights their potential for developing diagnostic and therapeutic approaches to mitigate renal fibrosis and retard CKD progression. - Source: PubMed
Publication date: 2026/09/16
Doghish Ahmed SAbuelhaded KhaledAbdelaziz Moustafa MahmoudShafey Moaz MohsenBasiouny Mohamed SalahSayed Ghadir AElrebehy Mahmoud AMoustafa Yasser MAbdel Mageed Sherif SAshour Mohamed MMohammed Osama AAli Rabab AHemdan Mohamed - Chronic hepatitis B virus (CHB) infection remains a major cause of hepatocellular carcinoma (HCC), yet the premalignant microenvironment that links to HBV-associated HCC (HBV-HCC) is still poorly defined. This review synthesizes evidence that HBV-infected hepatocytes function as signaling hubs that, through microRNA (miRNA)-regulated crosstalk with Kupffer cells, liver sinusoidal endothelial cells, hepatic stellate cells and cancer-associated fibroblasts (CAFs), progressively remodel the liver from an antiviral tissue into a premalignant and early tumor microenvironment. Across the HBV-HCC continuum, a core set of dysregulated miRNAs, including miR-21, miR-29a/b, miR-122, miR-146a, miR-155, miR-200a, miR-126, miR-210 and the miR-130/301 family, coordinates transition from innate antiviral responses to HSC activation, extracellular matrix deposition, mechanotransduction, angiogenesis, chronic inflammation and cancer-associated CAF programing. By mapping these stage-specific miRNA networks onto acute infection, CHB, early fibrogenesis, advanced fibrosis and CAF-rich dysplastic states, the review reframes HBV-HCC pathogenesis as a sequence of miRNA-guided hepatocyte-stromal states rather than a purely hepatocyte-intrinsic process. This perspective suggests that composite, cell-type-resolved miRNA signatures in serum or liver tissue could serve as biomarkers for identifying CHB patients who are entering a premalignant microenvironment before conventional surveillance markers become abnormal. It further highlights miRNA hubs that couple antiviral, fibrogenic, angiogenic and CAF-associated signaling as potential therapeutic targets for reprograming the HBV-driven premalignant microenvironment, with the long-term goal of intercepting HBV-HCC development at earlier, microenvironmentally defined stages. - Source: PubMed
Publication date: 2026/08/24
Sartorius KurtKramvis AnnaChuturgoon Anil - Ischemic heart disease (IHD) remains a leading global cause of death, sustained by microvascular dysfunction and defective endogenous repair despite revascularization. Endothelial progenitor cells (EPCs) were initially proposed as regenerative mediators, but direct cell therapy is constrained by poor engraftment, phenotypic heterogeneity, and safety concerns. Accumulating evidence establishes EPC-derived extracellular vesicles (EPC-EVs) as the principal effectors of vascular repair. These vesicles deliver bioactive cargo-including miR-126, miR-210, lncRNAs, and proteins that activate VEGF/PI3K/AKT/eNOS signaling in endothelial cells, promote angiogenesis and endothelial survival, attenuate apoptosis and ferroptosis, and induce reparative M2 macrophage polarization. Compared with cell therapy, EPC-EVs offer superior stability, lower immunogenicity, and manufacturing control as a cell-free platform. Translational challenges persist, including inconsistent EPC definitions, isolation variability, absence of validated potency assays linked to cardiovascular endpoints, and limited long-term safety data. Engineering strategies such as hypoxic preconditioning and targeted delivery may facilitate clinical translation of EPC-EV therapy for IHD. - Source: PubMed
Publication date: 2026/09/09
Han QilingWang XinmeiZhao Houjin - - Source: PubMed
Publication date: 2026/09/04
Yang FangYan YuboYang YangHong XuanWang MengYang ZhaoyangLiu BaogangYe Leiguang - Oral squamous cell carcinoma (OSCC) is characterized by late-stage diagnosis and high recurrence rates. Intratumoral hypoxia, driven by hypoxia-inducible factors 1α and 2α (HIF-1α/HIF-2α), orchestrates aggressive phenotypes including epithelial-mesenchymal transition (EMT), metabolic reprogramming, stemness maintenance, and therapeutic resistance. Non-coding RNAs (ncRNAs) serve as central post-transcriptional regulators of these hypoxic adaptations and offer promising non-invasive biomarker potential. - Source: PubMed
Publication date: 2026/08/17
Singh PoojaPandey Manoj