Histology and histopathology, Vol.41, Nº5, (2026)
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- PublicationOpen AccessCardioprotective mechanisms of Jiangfu Decoction against myocardial ischemia may involve regulation of the AMPK/PINK1/ Parkin mitochondrial autophagy pathway(2026) Yiwei Hao; Chen Li; Haoying Li; Xue Han; Hefei Wang; Xi Chu; Zhiwei Su; Shijiang Sun; Yawei Zhao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Jiangfu Decoction (JFD) is a classical traditional herbal medicine used to clinically treat ischemic heart disease (IHD). Nonetheless, the influence of JFD on myocardial ischemia (MI), along with its precise underlying mechanism, is still unclear. The objective of this research was to investigate the potential mechanisms by which JFD exerts cardio protective effects on MI induced by isoproterenol (ISO). Methods. An acute MI model was established by subcutaneous injection of ISO (85 mg/kg/d). To evaluate alterations in myocardial structure, electrocardiogram recordings and heart histology examinations were employed. The myocardial ultrastructure was observed by transmission electron microscopy (TEM). Using specific kits, the levels and activities of oxidative stress markers as well as inflammatory cytokines were separately assessed. Western blotting was employed to assess the expression levels of proteins related to adenosine monophosphate activated protein kinase (AMPK), PTEN-induced putative kinase 1 (PINK1), Parkin, Nod-like receptor protein 3 (NLRP3), and Caspase-1. Results. The findings show that JFD treatments markedly diminished heart rate, pathological alterations in cardiac tissue, chondriosome injury, and serum concentrations of creatine kinase, creatine kinasemyocardial band, lactate dehydrogenase, malon dialdehyde, interleukin-1β, and interleukin-18. Concurrently, these treatments augmented the activation of superoxide dismutase, catalase, and glutathione peroxidase in the serum of animals subjected to ISO treatment. Additionally, JFD also reversed the ISO induced changes in the levels of AMPK, PINK1, Parkin, NLRP3, and Caspase-1. Conclusion. JFD exhibits a notable safeguarding influence on MI via a mechanism that involves regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway, inhibition of pyroptosis, and reduction of oxidative stress and inflammation.
- PublicationOpen AccessUnraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach(2026) Shihui Liu; Hejing Ruan; Yuzhe Cheng; Yan Qiao; Jiawei Wang; Xiaojun Liu; Chuanmiao Liu; Wen Zhao; Siyuan Wang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. This study aimed to identify key molecules that potentially mediate the mechanisms by which YAP deletion or inhibition attenuates liver fibrosis. Materials and Methods. C57BL/6 mice were divided into four groups: control, carbon tetrachloride (CCl4), CCl4-YAP-HKO, and CCl4-verteporfin (VP). RNA sequencing (RNA-seq) and proteomic analysis were conducted. Immunohistochemistry and western blotting were also performed to verify the differentially expressed genes (DEGs) identified through the multi omics approach. Human subjects were enrolled to further assess the identified DEGs. Results. In comparison with the CCl4 group, both the CCl4-YAP-HKO and CCl4-VP groups exhibited liver fibrosis regression. RNA-seq and proteomic analyses identified 12 commonly differentially expressed molecules. Immunohistochemistry and western blotting validated that heat shock protein 27 (HSP27), heat shock protein 70 (HSP70), and p62 expression were significantly reduced, and milk fat globule-epidermal growth factor 8 (MFGE8) expression was elevated in both the CCl4-YAP-HKO and CCl4-VP groups compared with the CCl4 group. Furthermore, plasma p62, HSP27, and HSP70 levels were increased with the occurrence of chronic hepatitis B and HBV-related cirrhosis, whereas MFGE8 levels were decreased. Spearman’s correlation analysis further illustrated a significant association between these biomarkers and YAP levels. Conclusions. This study identified HSP27, HSP70, p62, and MFGE8 as crucial YAP-related molecules involved in liver fibrosis.
- PublicationOpen AccessMorphological evidence of telocytes in DHEA-induced polycystic ovary syndrome model(2026) Mehmet Yüncü; Yurdun Kuyucu; Esma İşçel; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaPolycystic Ovary Syndrome (PCOS) is a condition causing histopathological alterations in the ovarian stroma. Telocytes (TCs) are specialized interstitial/stromal cells present in the connective tissue of various organs. In this study, we investigated the presence and spatial organization of TCs in the ovaries of a rat model of PCOS induced by dehydro epiandrosterone (DHEA). The ovarian tissues from both PCOS and control groups were stained using hematoxylin-eosin (H&E), Bielschowsky's silver stain, methylene blue, and toluidine blue for light microscopy analysis, and scanned digitally. Ovaries were marked with double-labeled immunofluorescence with CD34/estrogen receptor-α (ER-α) and vimentin/ progesterone receptor-A (PR-A) and evaluated with a confocal microscope. The ultrastructure and telopodes (TPs) of TCs were also examined by transmission electron microscopy. TCs were identified in both groups, localized within follicular walls, adjacent to follicles, in stromal regions distant from the follicles, and perivascular areas. CD34/ER-α and vimentin/PR-A cells were significantly increased in PCOS. In conclusion, TCs were preserved in the DHEA-induced PCOS model, and according to our quantitative analysis, their ultrastructural features were unaffected by the PCOS microenvironment. Our findings suggest a potential association between TCs and the pathophysiology of PCOS. Further studies are necessary to elucidate the functional relationship of TCs in the development and progression of PCOS.
- PublicationOpen AccessRole of connexin 43 in odontogenesis and odontogenic tumors(2026) Ronell Bologna Molina; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaConnexin 43 (Cx43) is a transmembrane protein forming gap junctions essential for intercellular communication, regulating ion and molecule exchange, and coordinating key developmental and pathological processes. In odontogenesis, Cx43 expression in ameloblasts and odontoblasts orchestrates differentiation, mineralization, and tissue repair. Its dynamic regulation influences enamel and dentin formation, while altered expression is linked to defective tooth development. Beyond dental tissues, Cx43 participates in craniofacial morphogenesis and bone remodeling. In odontogenic tumors, Cx43 shows heterogeneous expression patterns, reflecting its role in tumor architecture, differentiation, and aggressiveness. High mesenchymal expression is seen in ameloblastic fibromas and fibro-odontomas, whereas follicular ameloblastomas and odontogenic keratocysts exhibit downregulation, particularly in basal cells, correlating with increased proliferation, anti apoptosis, and autophagy markers. These variations in odontogenic tumors suggest that Cx43 may act as a tumor suppressor by maintaining epithelial organization and regulating cell polarity. Molecularly, Cx43 interacts with MAPK/ERK, PI3K/AKT, and Wnt/β-catenin pathways, influencing cell cycle control, apoptosis, and epithelial-mesenchymal interactions. Loss of Cx43 disrupts gap junctional intercellular communication, potentially enhancing tumor progression. Therapeutically, modulating Cx43 could inhibit tumor angiogenesis, restore normal growth control, and promote differentiation toward less aggressive phenotypes. However, given its dual role in tumor suppression and tissue repair, targeted interventions must be context specific. Cx43 emerges as a promising diagnostic, prognostic, and therapeutic biomarker in different neoplasias, warranting further investigation to optimize clinical applications. The objective of this work is to review current information on the role of CX43 in normal tissue and odontogenic tumors to evaluate its possible usefulness as a future therapeutic target.
- PublicationOpen AccessTargeting thrombin with hirudin alleviates paraquat-induced pulmonary fibrosis via the PAR-1-mediated TGF-β1 pathway(2026) Weijuan Liu; Guowen Zheng; Zhaojun Song; Zike Zhang; Xiao Hu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Paraquat (PQ)-induced pulmonary fibrosis (PF) is a serious disease without specific antidotes. Thrombin is important for promoting fibrosis development. We aimed to explore whether thrombin promotes PQ-induced PF by activating the protease-activated receptor-1 (PAR-1)-mediated transforming growth factor-β1 (TGF-β1) pathway. Methods. Male Sprague Dawley rats received PQ treatment, either alone or with thrombin or hirudin (a thrombin inhibitor) (n=9 in the control, model, thrombin, and hirudin groups). After 7 or 14 days of treatment, oxidative stress (OS) indicators and histopathological damage in the lungs were detected. PF degree was evaluated using Masson staining and hydroxyproline levels in lung tissues and collagen levels in bronchoalveolar lavage fluid. Furthermore, type I collagen (Col-1), TGF-β1, and PAR-1 expression, as well as extracellular signal-regulated kinase 1/2 (ERK1/2) and mothers against decapentaplegic homolog 3 (Smad3) phosphorylation in the lungs, were assessed. To investigate the mechanism of thrombin on PQ induced PF, rats treated with PQ and thrombin further received SCH79797 (a PAR-1 inhibitor) alone or combined with SRI-011381 (a TGF-β agonist) (n=9 in the thrombin+SCH79797 and thrombin+SCH79797+ SRI-011381 groups). In addition to Masson staining and detection of the above-mentioned genes and proteins, alpha-smooth muscle actin (α-SMA), TGFβ receptor type I (TβRI), and type II (TβRII) expression in the lungs were also detected. Results. Both 7 and 14 days of thrombin treatment triggered OS, exacerbated lung histopathological damage, and promoted PF in PQ-stimulated rats. Furthermore, thrombin upregulated Col-1, TGF-β1, and PAR-1 expression as well as ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats. However, hirudin produced the opposite results. Additionally, the role of thrombin in promoting PF, increasing Col-1, TGF-β1, α SMA, PAR-1, TβRI, and TβRII expression and ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats was reversed by SCH79797, while the inhibitory effects of SCH79797 were counteracted by SRI-011381. Conclusions. Thrombin may promote PQ-induced PF by activating PAR-1-mediated TGF-β1, suggesting that PAR-1-mediated TGF-β1 is a potential target for preventing PQ-induced PF.
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