Mouse pre-microRNA Expression Construct mir-192
- Known as:
- Mouse pre-microRNA Expression Construct mir-192
- Catalog number:
- mmir-192-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-192
Related genes to: Mouse pre-microRNA Expression Construct mir-192
- Gene:
- MIR192 NIH gene
- Name:
- microRNA 192
- Previous symbol:
- MIRN192
- Synonyms:
- hsa-mir-192
- Chromosome:
- 11q13.1
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-18
Related products to: Mouse pre-microRNA Expression Construct mir-192
Related articles to: Mouse pre-microRNA Expression Construct mir-192
- Type 2 diabetes mellitus (T2DM) is a major driver of chronic kidney disease and cardiovascular morbidity worldwide. Extracellular vesicles (EVs), particularly exosomes, carry microRNAs (miRNAs) that reflect the pathophysiological state of their parent cells and represent promising non-invasive biomarkers. This review comprehensively examines the diagnostic and mechanistic roles of EV-derived miRNAs in diabetic nephropathy (DN) and cardiovascular diseases (CVDs) associated with T2DM. A PRISMA-guided literature search of PubMed, Scopus, Web of Science, and Embase identified 847 articles published between January 2020 and June 2026, of which 156 studies met the inclusion criteria. Several urinary exosomal miRNAs demonstrated significant diagnostic performance for DN, including miR-4534 (AUC = 0.786), miR-136-5p (sensitivity 72.2%, specificity 78.4%), and miR-142-3p. A meta-analysis of circulating miRNAs in diabetic kidney disease reported a pooled AUC of 0.79. In the cardiovascular setting, exosomal miR-155-5p (AUC = 0.901), miR-15a-3p (AUC = 0.874), and a four-miRNA panel (miR-433-3p/let-7b/miR-30-5p/miR-122-5p; AUC = 0.833) demonstrated strong diagnostic performance for ischemic heart disease and carotid atherosclerosis in T2DM. Mechanistically, key EV-associated miRNAs, including miR-21, miR-192, and the anti-fibrotic miR-29 family, participate in fibrosis, inflammation, oxidative stress, endothelial dysfunction, and cardiac remodeling pathways. EV-derived miRNAs therefore represent highly promising non-invasive biomarkers for the early diagnosis and monitoring of diabetic renal and cardiovascular complications. However, clinical translation requires standardized EV isolation and miRNA detection protocols, together with validation in large multicenter prospective cohorts. This review highlights the considerable diagnostic and translational potential of EV-derived miRNAs for precision medicine and liquid biopsy applications in T2DM complications. - Source: PubMed
Publication date: 2026/06/20
Arailym YessenbekovaAbaildayev ArmanAyaz Belkozhayev - Obesity and metabolic dysfunction associated steatotic liver disease (MASLD) are interrelated metabolic disorders characterized by chronic inflammation, insulin resistance, and dyslipidemia. While both conditions are well recognized clinically, the molecular mechanisms underlying their frequent coexistence remain poorly understood. Growing evidence indicates that circulatory exosomal microRNAs (miRNAs) act as critical mediators of inter-organ communication. In this PROSPERO-registered systematic review (CRD420251017335), we integrated clinical evidence with bioinformatics analyses to clarify shared miRNA-mediated regulatory networks between obesity and MASLD. Literature was retrieved from MEDLINE, ISI Web of Science, and Embase. Bioinformatics analysis using miRWalk also revealed shared miRNAs, predicted target genes, and elucidated enriched pathways using Gene Ontology and KEGG. Clinical studies identified 93 obesity-associated and 24 MASLD-associated exosomal miRNAs, with and emerging as common nodes. Bioinformatics analysis using miRWalk revealed extensive overlap at the functional level, including 40,410 shared miRNA-mRNA interactions and 42 common target genes. Several circulating exosomal miRNAs from obese individuals, including , , , and , were consistently associated with liver histopathology, inflammatory markers, and liver enzyme levels. Importantly, obesity-derived , , and showed strong diagnostic performance (AUC ≥ 0.85), exceeding that of alanine aminotransferase (ALT). Furthermore, emerged as a central therapeutic target within the shared miRNA network, regulated by both and , providing a molecular link between adipose tissue dysfunction and hepatic metabolic regulation. This integrative analysis supports a unified model in which exosomal miRNAs serve as key molecular intermediaries connecting obesity and MASLD. - Source: PubMed
Publication date: 2026/05/22
Mo QiguiGhafourian AmirrezaHamdi MasoomehAlidadipour ArianSoleimani MahdiehDavoudi MaryamMiao XiaoleiAfrisham RezaBagherieh Molood - Albuminuria is a widely used clinical marker for diabetic nephropathy (DN); however, its limited sensitivity and specificity in detecting early renal alterations highlight the need for additional indicators. MicroRNAs (miRNAs) are emerging as molecular regulators involved in the pathogenesis of DN and may provide insight into early renal involvement in type 2 diabetes mellitus (T2DM). This study aimed to evaluate the serum expression levels of miR-21 and miR-192 in normo- and microalbuminuric patients with T2DM, and explore their associations with metabolic and renal parameters. - Source: PubMed
Abd Alrahim Nosaiba MAbd Elalim Alshaymaa AFarrag Enas AAbdel-Kareem Shimaa MShaban Sahar SaadEldeenEldamanhory Aya AKasim Sammar AhmedFath Allah Radwa MMayah Fatma IGhamry Aya AAlkhawagah Sabah MKhidr Emad Gamil - Alcohol consumption is a modifiable, dose‑dependent risk factor that accelerates cancer initiation, progression, and therapy resistance across breast, liver, colorectal, esophageal, and melanoma cancers. Alcohol metabolism generates acetaldehyde, a genotoxic metabolite that induce DNA damage and impairs repair; drives oxidative stress, hormonal imbalance and promoting a tumor‑supportive microenvironment. These effects are amplified by obesity and insulin resistance, which heighten aggressiveness and blunt treatment response. Alcohol reshapes the tumor immune microenvironment (TIME) and undermines therapies, including immunotherapy. It impairs dendritic cell antigen presentation and co‑stimulation, limits CD4⁺/CD8⁺ priming, and expands immunosuppressive MDSCs and M2‑like TAMs that inhibit cytotoxic T cells and express checkpoint ligands. Concurrent cytokine shifts (TNFα, IL‑6), persistent ROS-NF‑κB signaling, and stromal/vascular remodeling promote immune exclusion and weaken responses to checkpoint blockade, targeted agents, and chemotherapy. Alcohol‑related gut dysbiosis is linked to ICB responsiveness-dampens antitumor immunity. Alcohol increases exosome biogenesis; circulating vesicles enriched in hepatocyte and inflammatory miRNAs (e.g., miR‑122, miR‑192) reprogram immune signaling and metastasis, forming a vesicular axis linking exposure to TIME dysfunction and resistance. Risk is synergistic with tobacco and worsens with aging as detoxification and DNA repair decline. Sex‑specific pharmacokinetics and composition confer vulnerability in women, while socioeconomic barriers delay diagnosis and care. Personalized prevention strategies that incorporate alcohol reduction, smoking cessation, and nutritional support, with emerging biomarkers such as exosomal miRNAs and alcohol‑related metabolites for early detection and risk stratification, are needed to mitigate alcohol‑related carcinogenesis, given the lack of definitive human evidence on alcohol's independent effects on immunotherapy and chemotherapy efficacy. - Source: PubMed
Publication date: 2026/04/29
Deshpande Ravindra PramodTyagi AbhishekWatabe Kounosuke - Nile tilapia (Oreochromis niloticus) is one of the most important aquaculture species worldwide, but its sensitivity to low temperatures limits production, particularly in subtropical and temperate regions. Since somatic growth in fish is largely regulated by the growth hormone/insulin-like growth factor (GH/IGF) axis, and microRNAs contribute to the post-transcriptional regulation of growth, metabolism, and stress responses, this study investigated the molecular effects of chronic cold exposure in Nile tilapia by analysing growth-related genes and five candidate microRNAs (miR-192, miR-206, miR-133, miR-125b, and miR-30b) in the brain, liver, and hindgut after 28 days at 15 °C. Cold exposure induced marked tissue-specific transcriptional changes. In the liver and hindgut, gh1, igf-1, and igf-2 were generally upregulated, whereas in the brain gh1 expression increased while ghra, igf-1, and igf-2 were reduced. MicroRNA expression also differed among tissues: in the brain, miR-192 and miR-206 were upregulated and miR-125b was downregulated; in the liver, miR-133 and miR-206 increased whereas miR-192 decreased; and in the hindgut, miR-192, miR-125b, and miR-206 were downregulated. The concurrent upregulation of miR-206 and igf-1 in the liver suggests a complex and tissue-dependent regulatory relationship under cold stress. Overall, these findings demonstrate that chronic low-temperature exposure modulates both the GH/IGF axis and miRNA expression in a tissue-specific manner, highlighting integrated transcriptional and post-transcriptional mechanisms involved in cold adaptation. This study provides new insight into the molecular basis of thermal resilience in Nile tilapia and supports the identification of candidate biomarkers for cold tolerance in aquaculture. - Source: PubMed
Publication date: 2026/04/10
Dellagostin Eduardo NGonçalves Natiéli MBlödorn Eduardo BMartins Amanda W SRattmann Guilherme N LVasconcelos Kaylane PCollares Gilberto LSilveira Tony L RRemião Mariana HCampos Vinicius F