Journal of Molecular Histology最新文献

{"title":"Chia seed oil attenuates titanium dioxide nanoparticles-induced ulcerative colitis in rats through suppression of NLRP3 inflammasome pathway “Histological and Molecular Study”","authors":"Nahla Reda Sarhan,&nbsp;Amira I. Shrief,&nbsp;Rasha Elmowafy,&nbsp;Sally A. Elekhtiar","doi":"10.1007/s10735-026-11007-7","DOIUrl":"10.1007/s10735-026-11007-7","url":null,"abstract":"<div><p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease. Titanium dioxide nanoparticles (TiO₂ NPs) are used as a whitening agent in food industry and considered a risk factor for UC. Chia seed oil is nutrient-rich oil with antioxidant and anti-inflammatory properties. NOD-like receptor pyrin domain-containing protein 3 (NLRP3) detects danger signals forming NLRP3 inflammasome complex. This study assessed the attenuating effect of chia seed oil against TiO₂ NPs-induced UC. Forty-eight adult male rats were divided into 4 groups; control, chia: received oral chia seed oil (2.5 ml/kg/day) for 3 weeks, TiO₂: received TiO₂ NPs (100 mg/kg) orally for 2 weeks and TiO₂+chia group: received chia seed oil for 1 week before TiO₂ NPs and continued for 2 weeks. Colon specimens were dissected out for histological and molecular analysis (RT-qPCR) and evaluation of oxidative stress. Serum level of inflammatory cytokines was also measured. Compared to TiO₂ group, TiO₂+chia group showed amelioration of histological changes as preservation of crypts and goblet cell number, attenuation of inflammation, maintenance of junctions, decreased percentage area of fibrosis, Bax, interleukin-1β and proliferating cell nuclear antigen immunostaining. Together with reduced lipid peroxidation, enhanced antioxidant enzymes, downregulation of NLRP3, caspase-1 and interleukin-1β gene expression and reduction of serum inflammatory cytokines. In conclusion, chia seed oil attenuates TiO₂ NPs-induced UC damage through reduction of oxidative stress, downregulation of NLRP3 inflammasome pathway, altered pro-apoptotic signaling, inhibition of fibrosis and cell proliferation; and epithelial barrier preservation. So, it could serve as a prophylactic agent or adjuvant therapy for UC.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149235142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive insight into the anti-dyslipidemic and pancreatic lipase inhibition activities of Clematis flammula L. and Fraxinus angustifolia Vahl. extracts using two animal models","authors":"Adlane Zaidi,&nbsp;Dina Atmani-Kilani,&nbsp;Djebbar Atmani,&nbsp;Kenza Moulaoui,&nbsp;Naima Saidene,&nbsp;Nassima Chaher-Bazizi","doi":"10.1007/s10735-026-11011-x","DOIUrl":"10.1007/s10735-026-11011-x","url":null,"abstract":"<div><p><i>Clematis flammula</i> and <i>Fraxinus angustifolia</i> leaves are commonly used in Algeria to treat inflammatory diseases, with potential hypolipidemic effects that have not been investigated so far. The present study explored the in vitro, ex vivo, and in vivo hypolipidemic effects of ethanolic leaf extracts from both plants using two animal models (mice and rabbits) with distinct lipid metabolism. Dyslipidemia was induced by oral administration of Triton X-100, once daily for three consecutive days. Immediately after each Triton X-100 administration, animals received plant extracts (100 and 200 mg/kg bw) or atorvastatin (10 mg/kg bw). Anti-lipase and anti-HMG-CoA reductase activities were evaluated using in vitro and ex vivo assays. Triton X-100 induced marked alterations in serum lipid profiles, characterized by increased LDL-C, VLDL-C, and total cholesterol levels, which were improved by <i>C. flammula</i> and <i>F. angustifolia</i> extracts, particularly at 200 mg/kg bw. While <i>F. angustifolia</i> exhibited greater hypolipidemic efficacy, the lack of improvement in total cholesterol in mice treated with <i>C. flammula</i>, in contrast to rabbits, may suggest species-dependent differences in lipid metabolism, potentially involving CETP-mediated cholesterol transport, which requires further experimental confirmation. In vitro anti-lipase assays showed greater inhibitory potency for <i>F. angustifolia</i> (IC50 = 3.55 µg/mL) than <i>C. flammula</i> (IC50 = 12.10 µg/mL). Both extracts inhibited HMG-CoA reductase activity by over 60% in vitro and ex vivo, with IC50 values of 90.06 and 96.57 µg/mL for <i>F. angustifolia</i> and <i>C. flammula</i>, respectively. Histological examination further supported the hypolipidemic effects of both extracts. Overall, these findings highlight <i>C. flammula</i> and <i>F. angustifolia</i> as promising natural sources of bioactive compounds with potential applications in managing hypercholesterolemia and dyslipidemia.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149234895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aqueous extract of Ormocarpum cochinchinense promotes fracture healing through coordinated angiogenic, osteogenic, and cytoprotective mechanisms","authors":"Preethi Vincent,&nbsp;Arun Pugazhendi,&nbsp;Vishnugurubaran Dhanakaran,&nbsp;Krishna Priya Mani","doi":"10.1007/s10735-026-11003-x","DOIUrl":"10.1007/s10735-026-11003-x","url":null,"abstract":"<div><p><i>Ormocarpum cochinchinense</i> has long been used in traditional medicine for the management of bone fractures. Despite its widespread ethnomedicinal use, scientific evidence supporting its efficacy and underlying mechanisms in fracture healing remains limited. This study aimed to investigate the safety and fracture-healing potential of the aqueous extract of <i>O. cochinchinense</i> (OCE) with emphasis on angiogenesis and osteogenesis, and to elucidate its role in modulating endothelial cell inflammation. The biological activity of OCE was assessed using a combination of in vitro and in vivo approaches. The phytochemical characterization of the extract was performed using GC–MS analysis. The safety profile of OCE was assessed through in vivo toxicity evaluation and the fracture-healing efficacy was investigated through radiographic and histological analyses. Molecular mechanisms were examined by assessing the expression of angiogenic and osteogenic marker genes. Additionally, endothelial protective effects were evaluated under lipopolysaccharide (LPS)-induced inflammatory conditions by measuring oxidative stress markers and pro-inflammatory mediators. GC–MS analysis identified a total of 25 phytocompounds in OCE. OCE exhibited no observable toxicity in rats. It accelerated fracture healing by promoting advanced callus formation, enhancing collagen-rich matrix deposition, and improving mineralization. OCE significantly upregulated angiogenic (VEGFA, VEGFR2) and osteogenic (BMP2, SP7, RUNX2, ALP, Col1A1, OPN, OCN) gene expression, indicating coordinated activation of bone regeneration pathways. Furthermore, OCE protected endothelial cells from LPS-induced cytotoxicity by reducing reactive oxygen species and nitric oxide levels and downregulating inflammatory mediators including NOX1, NOX2, NOX4, iNOS, IL-1β, IL-6, and TNF-α. OCE promoted fracture healing through a multifaceted mechanism involving enhanced angiogenesis and osteogenesis. It also confers endothelial protection by mitigating inflammation and oxidative stress that might aid in improved endothelial function and thereby fracture healing. These findings validate its traditional use and highlight its potential as a safe and effective natural therapeutic agent for bone regeneration.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149226878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of topical vildagliptin versus triamcinolone acetonide on experimentally induced hypertrophic scars in a rabbit model","authors":"Zaynab Ali Nasser,&nbsp;Farrah Rasool Jaafar","doi":"10.1007/s10735-026-11017-5","DOIUrl":"10.1007/s10735-026-11017-5","url":null,"abstract":"<div><p>The present study aimed to evaluate the effects of topical vildagliptin on experimentally induced hypertrophic scars (HTSs) in a rabbit model. A total of 40 healthy male albino rabbits were randomly assigned to five groups (<i>n</i> = 8): healthy control (CTRL), untreated induced HTS model (HTS model), vehicle-received (VEH), 0.1% triamcinolone acetonide-treated (TAC), and 3% vildagliptin-treated (VIL). On day 0, four full-thickness wounds extending to the cartilage were created on the ventral surface of each rabbit ear using an 8-mm biopsy punch. On day 30, topical treatment was initiated on the newly formed scars and continued twice daily for 21 days. Samples were collected on day 51 post-wounding. Outcome measures included molecular quantification of collagen type 1 (Col I), collagen type 3 (Col III), transforming growth factor-beta 1 (TGF-β1), interleukin 6 (IL-6), histopathological examination, and alpha-smooth muscle actin (α-SMA) immunoreactivity. Vildagliptin significantly reduced Col I, Col III, TGF-β1, and IL-6 compared with the HTS model group (<i>p</i> &lt; 0.001). Histopathological analysis revealed a marked improvement in scar architecture, as evidenced by lower histopathological scores and a reduced scar elevation index. Masson’s trichrome (MT) staining demonstrated a significant reduction in collagen deposition, accompanied by partial restoration of normal collagen fiber organization. Immunohistochemical analysis revealed no significant change in α-SMA immunoreactivity. This more likely reflects a potential incomplete suppression of myofibroblasts. Overall, these findings suggest that topical vildagliptin may represent a promising therapeutic approach for the treatment of HTSs.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149226907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hybrid siamese heterogeneous convolutional neural networks with electric eel foraging optimization-based deep feature vectors concatenation for eye disease detection","authors":"K. R. N. Aswini,&nbsp;S. B. Mohan,&nbsp;K. Selvam,&nbsp;S. Leoni Sharmila","doi":"10.1007/s10735-026-10974-1","DOIUrl":"10.1007/s10735-026-10974-1","url":null,"abstract":"<div><p>In order to prevent vision loss and blindness, eye problems must be identified and diagnosed. In order to avoid blindness and vision loss, it is crucial to identify the main cause of eye illness. In previous studies, several DL algorithms have been used for detecting eye disease but do not provide sufficient results. To overcome these challenges is suggested. In this publication, a Hybrid Siamese Heterogeneous Convolutional Neural Network with Electric eel foraging optimization-based Deep Feature Vectors Concatenation for Eye Disease Detection (DeepSiaHetCNN-EeFOA) is suggested. There are datasets like databases similar datasets. These data are subsequently preprocessed using the Kuwahara Filtering with Anisotropic Dissemination (KFAD) technique. The Unet with split attention-based MobileNetV2 network (U-SA-MNetV2) approach is then used to segment eye diseases and extract features. DeepSiaHetCNN-EeFOA is then used for classifications to identify normal and abnormal areas and to identify the kind of eye illness. The system demonstrated was run using Python. The proposed DeepSiaHetCNN-EeFOA is tested on four datasets. It outperforms existing approaches by achieving 99.9% accuracy &amp; 99.8% recall. This demonstrates the method’s exceptional effectiveness and promise for further development in the sector.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149226931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lycopene inhibits proliferation, induces apoptosis, and suppresses migration in cervical cancer cells: involvement of PI3K/Akt signaling","authors":"Zaira Colín-Val,&nbsp;Luis-Alberto Reyes-Nava,&nbsp;Diana A. García,&nbsp;Daniel Beltrán-Isabeles,&nbsp;Gabriel Herrera-Maya,&nbsp;Rebeca López-Marure","doi":"10.1007/s10735-026-10964-3","DOIUrl":"10.1007/s10735-026-10964-3","url":null,"abstract":"<div><p>Cervical cancer remains a major cause of mortality worldwide, highlighting the need for alternative therapeutic strategies. Lycopene, a dietary carotenoid with known antioxidant properties, has demonstrated anticancer activity in several malignancies; however, its mechanistic effects in cervical cancer remain poorly understood. We hypothesize that lycopene inhibits the growth of cervical cancer cell lines and certain cancer-related processes. Therefore, we performed an in vitro study to investigate lycopene's effects on proliferation, viability, migration, and apoptosis in three cervical cancer cell lines (HeLa, SiHa, and ViBo) using lycopene concentrations ranging from 1.25 to 40 µM, and further evaluated the underlying mechanisms using 2.5 and 40 µM lycopene, and evaluated its effects on non-malignant cardiomyoblasts (H9c2). Lycopene significantly reduced proliferation and cell viability and impaired migration in all cancer cell lines. Flow cytometry revealed increased apoptosis, associated with time-dependent modulation of the Bax/Bcl-2 ratio and caspase-3 activation. Mechanistically, lycopene decreased Akt phosphorylation without affecting total Akt or PI3K levels, indicating the participation of the PI3K/Akt survival pathway. Importantly, pharmacological PI3K inhibition with wortmannin supported this pathway's involvement in mediating lycopene-induced effects. Notably, lycopene at lower concentrations showed minimal cytotoxicity in H9c2 cells, suggesting some selectivity toward cancer cells. Together, these findings show that lycopene decreases proliferation and viability, promotes apoptosis, and suppresses migration in cervical cancer cells; these effects were associated with PI3K/Akt signaling, indicating that this pathway may contribute to its anticancer effects and highlighting lycopene's potential as a therapeutic candidate.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><img></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149189737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin-(1–7) attenuates collagen-induced arthritis and suppresses ferroptosis in THP-1-derived macrophages: involvement of p53/SLC7A11 signaling","authors":"Haojun Yang,&nbsp;Anting Liu,&nbsp;Min Sheng,&nbsp;Shan Zhang,&nbsp;Lin Tang","doi":"10.1007/s10735-026-11009-5","DOIUrl":"10.1007/s10735-026-11009-5","url":null,"abstract":"<div><p>Rheumatoid arthritis (RA) is characterized by persistent synovial inflammation and progressive joint destruction, while ferroptosis has emerged as a potential contributor to inflammatory tissue injury. This study investigated whether angiotensin-(1–7) [Ang-(1–7)] attenuates arthritis by regulating ferroptosis and explored the involvement of p53/solute carrier family 7 member 11 (SLC7A11) signaling. Bioinformatic analysis of the GSE55235 dataset was performed to identify ferroptosis-related differentially expressed genes in RA. A collagen-induced arthritis (CIA) mouse model and erastin-treated THP-1-derived macrophages were used to evaluate the effects of Ang-(1–7) in vivo and in vitro. Ferroptosis-related genes in RA were enriched in inflammatory responses, oxidative stress, ferroptosis, and p53 signaling. In CIA mice, Ang-(1–7) reduced paw swelling and arthritis scores, ameliorated synovial inflammation and joint damage, and attenuated iron deposition, lipid peroxidation, and ferroptosis-related molecular alterations. Double-immunofluorescence staining further demonstrated decreased glutathione peroxidase 4 (GPX4) and increased acyl-CoA synthetase long-chain family member 4 (ACSL4) expression in F4/80-positive macrophage areas in CIA joints, both of which were reversed by Ang-(1–7). In erastin-treated THP-1-derived macrophages, Ang-(1–7) improved cell viability, restored glutathione levels, reduced malondialdehyde, reactive oxygen species, lipid reactive oxygen species, and Fe²⁺ accumulation, alleviated mitochondrial injury, and reversed ferroptosis-related molecular abnormalities. Nutlin-3 A-mediated p53 stabilization partially weakened these protective effects, whereas TP53 knockdown diminished the additional protective response to Ang-(1–7). These findings suggest that Ang-(1–7) attenuates ferroptosis-related joint injury in CIA mice and suppresses erastin-induced ferroptosis in THP-1-derived macrophages, with these effects being partially associated with modulation of p53/SLC7A11 signaling.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149189933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network pharmacology-based investigation on the mechanism of aloin in ameliorating atherosclerosis by regulating macrophage polarization","authors":"Ye Tian,&nbsp;Xianghui Mei,&nbsp;Fang Zeng,&nbsp;Baichao Li,&nbsp;Wentao Du,&nbsp;Xianru Chen","doi":"10.1007/s10735-026-11004-w","DOIUrl":"10.1007/s10735-026-11004-w","url":null,"abstract":"<div><p>Atherosclerosis (AS) is a chronic inflammatory vascular disease in which macrophage polarization plays a pivotal role in plaque progression and stability. Aloin, a major anthraquinone compound isolated from Aloe vera, possesses potent anti-inflammatory activities; however, its therapeutic potential and underlying mechanisms in AS remain insufficiently understood. In the present study, a network pharmacology approach combined with molecular docking, cellular experiments, and animal validation was employed to investigate the protective effects of aloin against AS and elucidate its molecular mechanism. Common targets shared by aloin, macrophage polarization, and AS were identified, followed by protein–protein interaction network construction and GO/KEGG enrichment analyses. Molecular docking demonstrated strong binding affinities of aloin toward key inflammatory targets, particularly NF-κB and STAT3. Experimental validation showed that aloin significantly suppressed nitric oxide production in lipopolysaccharide-induced RAW264.7 macrophages and inhibited M1 macrophage polarization while promoting the M2 phenotype, as evidenced by decreased expression of iNOS and TNF-α and increased expression of Arg-1 and IL-10. In ApoE-/- mice fed a high-fat diet, aloin markedly reduced aortic plaque formation and alleviated vascular pathological injury. Mechanistically, both in vitro and in vivo analyses revealed that aloin significantly attenuated the phosphorylation of NF-κB and STAT3, thereby blocking activation of the NF-κB/STAT3 signaling pathway. Collectively, these findings suggest that aloin may contribute to the amelioration of atherosclerotic lesions by modulating macrophage polarization balance through inhibition of NF-κB/STAT3 signaling, highlighting its potential as a candidate worthy of further investigation for the prevention and treatment of atherosclerosis.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FAM43B mediates BMAL1-driven regulation of ERK signaling to promote cervical cancer progression","authors":"Chunyu Pan,&nbsp;Min Li","doi":"10.1007/s10735-026-11008-6","DOIUrl":"10.1007/s10735-026-11008-6","url":null,"abstract":"<div><p>Cervical cancer is a common malignant tumor of the female reproductive system, and patients with advanced and metastatic diseases have poor prognosis. It is urgent to explore novel molecular targets and regulatory mechanisms. As a core circadian rhythm factor, BMAL1 exerts tumor-suppressive or oncogenic effects in various malignancies, while its biological functions, downstream pathways and molecular mechanisms in cervical cancer remain largely unclear. In this study, human cervical cancer cell lines SiHa and HeLa, as well as nude mouse subcutaneous xenograft models were used as research systems. A series of experiments including transcriptome sequencing, protein interaction assay, ubiquitination detection, cellular functional experiments and in vivo animal assays were performed. The results demonstrated that BMAL1 knockdown markedly inhibited the proliferation, colony formation, invasion and migration of cervical cancer cells, and induced G1-phase cell cycle arrest. Transcriptome sequencing and KEGG pathway enrichment analysis identified the ERK signaling pathway as the major downstream pathway of BMAL1, and BMAL1 positively regulated the phosphorylation of key molecules in the ERK pathway. Mechanistically, BMAL1 specifically bound to FAM43B via its transactivation domain (TAD), promoted K63-linked ubiquitination of FAM43B, enhanced the protein stability of FAM43B. As a downstream effector, FAM43B unidirectionally activated the ERK signaling pathway, and no reverse regulatory loop existed between the two proteins. Silencing FAM43B significantly reversed the malignant phenotypes of cervical cancer cells. In vivo xenograft experiments further verified that BMAL1 knockdown suppressed tumor growth, reduced tumor proliferative activity. In summary, BMAL1 regulates the ERK signaling pathway by modulating the ubiquitination of FAM43B, thereby promoting the progression of cervical cancer. This study reveals a novel BMAL1/FAM43B/ERK regulatory axis and its underlying mechanism, providing potential molecular targets and experimental evidence for prognostic evaluation and targeted therapy of cervical cancer.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of miR-671-3p expression with clinical efficacy and complications in hemodialysis patients","authors":"Mei Yang,&nbsp;Jun Long,&nbsp;Yongxiu Luo,&nbsp;Guilin Chen,&nbsp;Li Wang,&nbsp;Li Wang,&nbsp;Dengfeng Kuang,&nbsp;Chunyan Wang,&nbsp;Shengling Shi","doi":"10.1007/s10735-026-10994-x","DOIUrl":"10.1007/s10735-026-10994-x","url":null,"abstract":"<div><p>Vascular calcification (VC) is a common and severe complication in hemodialysis patients, increasing the risk of major adverse cardiovascular events (MACE). This study aimed to explore the clinical value of miR-671-3p in hemodialysis patients and its regulatory role in VC. A total of 163 end-stage renal disease (ESRD) patients undergoing hemodialysis were enrolled, including 107 with VC and 56 without VC. Clinical data were used to evaluate the role of miR-671-3p in the diagnosis (ROC) and risk prediction (logistic regression) of VC and MACE. A high-phosphorus-induced human aortic smooth muscle cells (hASMCs) calcification model was established, and then cell viability (CCK-8), apoptosis rate (flow cytometry), calcium content, alkaline phosphatase (ALP) activity, and the levels of Runx2 and α-SMA were measured. Bioinformatics analysis and a dual-luciferase assay were employed to predict and validate the downstream target genes of miR-671-3p. miR-671-3p was downregulated in VC patients and showed high diagnostic value for VC. Its levels showed significant correlations with disease severity and could effectively predict the risk of MACE in VC patients. Overexpression of miR-671-3p markedly alleviated calcification-induced decreases in cell viability, increases in apoptosis and calcium content, upregulation of ALP and Runx2, and downregulation of α-SMA; however, this protective effect was reversed by overexpression of its downstream target FBXW2. miR-671-3p may serve as a promising candidate biomarker for diagnosing VC and predicting MACE in VC patients. miR-671-3p may attenuate the progression of VC by inhibiting calcification in hASMCs.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149176723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}