Tissue & cell最新文献

{"title":"TACC3 facilitates chondrocyte differentiation by attenuating abnormally activated FGFR3 signaling in achondroplasia − An in vitro study","authors":"Xiang Li ,&nbsp;Long Bao ,&nbsp;Xiaoyan Wang ,&nbsp;Haiying Wu ,&nbsp;Ting Chen ,&nbsp;Rongrong Xie ,&nbsp;Hui Sun ,&nbsp;Dandan Zhang ,&nbsp;Lili Wang ,&nbsp;Linqi Chen","doi":"10.1016/j.tice.2025.102940","DOIUrl":"10.1016/j.tice.2025.102940","url":null,"abstract":"<div><h3>Background</h3><div>Achondroplasia is a common form of dwarfism. It is caused by mutations in the fibroblast growth factor receptor 3 (FGFR3), which inhibits chondrocyte proliferation and differentiation.</div></div><div><h3>Aim</h3><div>In this study, we intended to investigate the underlying mechanism of FGFR3 mutation-induced chondrocyte differentiation defection.</div></div><div><h3>Method</h3><div>Insulin-transferrin-selenium (ITS-G) stimulated ATDC5 cells was used as an <em>in vitro</em> model. Alcian Blue staining was performed to detect ATDC5 cell differentiation.</div></div><div><h3>Results</h3><div>TACC3 expression was increased during ATDC5 cell differentiation. ITS-G induced ATDC5 cell differentiation was inhibited by the FGFR3 mutation, as evidenced by the decreased expression of ACAN and COL2A1. The downregulation of TACC3 expression induced by ITS-G stimulation was upregulated by FGFR3 overactivation. The TACC3 inhibitor (KHS101) promoted differentiation in FGFR3 mutant ATDC5 cells. The p38 signaling pathway has been implicated in FGFR3 mutation-induced chondrocyte differentiation defects. KHS101 promoted the expression of p38. KHS101-induced increase in ATDC5 cell differentiation was inhibited by the administration of a p38 inhibitor. These results suggest that TACC3 might play a role through the p38 signaling pathway in chondrocyte differentiation defects caused by FGFR3 mutations.</div></div><div><h3>Conclusion</h3><div>TACC3 might represent a novel target for achondroplasia.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102940"},"PeriodicalIF":2.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948007","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":"Oxygen-glucose deprivation induces actin spillover in brain endothelial cells","authors":"Yiyin Zhao ,&nbsp;Xiaojing Zhou ,&nbsp;Songbin He ,&nbsp;Jingjing Liu ,&nbsp;Meng Jin ,&nbsp;Jiaqian Li ,&nbsp;Lulan Pan ,&nbsp;Lin Zhou","doi":"10.1016/j.tice.2025.102946","DOIUrl":"10.1016/j.tice.2025.102946","url":null,"abstract":"<div><div>Stroke is the leading cause of death and disability worldwide, and the mechanisms of stroke onset have not been fully elucidated. The research investigated how actin remodeling functions within brain microvascular endothelial cells (bEnd.3 cell<span><span>²</span></span>) when exposed to glucose-oxygen deprivation (OGD<span><span>³</span></span>) circumstances. OGD exposure for 6 h in bEnd.3 cell led to increased F-actin polymerization and actin overflow into the supernatant which demonstrated a disruption of intracellular actin balance. This process is mainly mediated by the cofilin and myosin light chain (MLC<span><span>⁴</span></span>) phosphorylation. Jasplakinolide further enhanced F-actin polymerization, while Latrunculin B inhibited actin polymerization and alleviated cellular damage. In conclusion, our research has revealed the crucial role of actin overflow driven by cofilin and MLC signals in brain endothelial cell injury, providing new insights into the pathophysiology of stroke.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102946"},"PeriodicalIF":2.7,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890559","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":"Enhancing TB diagnosis: Improving specificity with scFv antibodies targeting the PPE17 epitope","authors":"Kamran Heidarnejad ,&nbsp;Mehrzad Bahtouee ,&nbsp;Seyed Nooreddin Faraji ,&nbsp;Setareh Moazen ,&nbsp;Farhad Abbasi ,&nbsp;Amirhossein Sahebkar ,&nbsp;Foroogh Nejatollahi","doi":"10.1016/j.tice.2025.102933","DOIUrl":"10.1016/j.tice.2025.102933","url":null,"abstract":"<div><h3>Background</h3><div>Serological assays have demonstrated enhanced simplicity, accuracy, and effectiveness in detecting Mycobacterium Tuberculosis (Mtb) antigens. The proline-proline-glutamic acid 17 (PPE17) antigen, specifically localized on the surface of Mtb, has been identified as unique to the Mtb species. The unique properties of single-chain antibodies make them well-suited for accurate diagnostic applications. In this study, specialized single-chain antibodies (scFvs) targeting PPE17 were employed to create a precise indirect immunofluorescent assay for diagnosing pulmonary tuberculosis (TB).</div></div><div><h3>Methods</h3><div>To select an immunodominant epitope of PPE17 in silico analysis was applied. The sequence was evaluated using the BLAST algorithm. A phage antibody display library of scFv was applied and two scFvs were isolated against the epitope by panning process. Specific clones were distinguished through PCR and DNA fingerprinting techniques. The reactivity of the chosen scFvs towards the selected epitope was assessed by ELISA. An Indirect Immunofluorescence Assay (IFA) was performed on 50 positive and 50 negative TB sputum smears, which were confirmed through both culture and genotype methods, to evaluate the performance of anti-PPE17 scFvs in accurately and rapidly detecting TB-positive smears, and TB-negative and Nocardia smears serving as negative controls for comparison.</div></div><div><h3>Results</h3><div>An immunodominant epitope of the PPE17 antigen consisting of amino acids 27–39, was identified. Two specific anti-PPE17-scFvs with frequencies of 25 % and 20 % were selected. ELISA results confirmed the reactivity of the scFvs against the epitope. Immunofluorescence assays demonstrated positive results for both antibodies when tested against positive TB sputum smears, whereas no positive results were obtained in tests against TB-negative and Nocardia smears.</div></div><div><h3>Conclusion</h3><div>A fast and accurate indirect immunofluorescence assay was developed to identify Mtb bacteria in TB sputum smears using specific anti-PPE17 scFvs. The results illustrated the capability of both scFvs in detecting Mtb in TB samples and differentiating Mtb from Nocardia smears. This suggests the potential for a novel diagnostic test that ensures precise TB detection in sputum samples, thereby preventing any potential misdiagnosis of tuberculosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102933"},"PeriodicalIF":2.7,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931516","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":"Tetracera asiatica flavonoids attenuate alcohol-induced liver injury by suppressing oxidative stress and inflammation mediated by the Keap-1/Nrf2/HO-1, NF-κB/MAPK and PERK/Nrf2 signaling pathways in alcoholic liver injury rats","authors":"Fang-fang Da ,&nbsp;Yao-ting Meng ,&nbsp;Yu-feng Chen ,&nbsp;Zi-wan Yuan ,&nbsp;Ying Liu ,&nbsp;Zhong-hua Dai","doi":"10.1016/j.tice.2025.102913","DOIUrl":"10.1016/j.tice.2025.102913","url":null,"abstract":"<div><div>Alcoholic liver disease is regarded as a leading reason for liver cirrhosis. This study aimed to investigate the protective effect of <em>tetracera asiatica flavonoids</em> (TAF) on alcoholic liver injury (ALI) and explore the associated mechanisms. An ALI rat model was established and then divided into four groups, including ALI group, low-dose TAF (l-TAF) group, medium-dose TAF (m-TAF) group, and high-dose TAF (h-TAF) group. Levels of ALT, AST, ALB, SOD, MDA, NO, CAT, TG, TNF-α, IL-1β, Nrf2, Keap1, HO-1, NQO-1, and GSH-Px were measured in ALI rats in different groups. Pathological changes and inflammatory infiltration were examined using HE staining. Western blot was used to detect expressions of Nrf2, MAPK p38, PERK, NF-κB, ERK1/2 and anti-JNK1/2/3. The results showed that TAF protected against alcoholic liver injury in ALI rats by decreasing ALT and AST levels and inhibiting inflammatory response. TAF significantly reversed alcohol-induced increase in NO (P &lt; 0.05), and remarkably decreased levels of TNF-α (<em>P</em> &lt; 0.001) and IL-1β (<em>P</em> &lt; 0.01), compared with the ALI group. TAF significantly increased the transcription of Nrf2, Keap1, HO-1, NQO-1 and GSH-Px gene (all P &lt; 0.05) and inhibited the alcohol-induced upregulation of MAPK p38 expression (<em>P</em> &lt; 0.001), p-NF-κB/NF-κB ratio (<em>P</em> &lt; 0.001), p-ERK/1/2/ERK1/2 ratio (<em>P</em> &lt; 0.05), and p-JNK1/2/3/JNK1/2/2 ratio (<em>P</em> &lt; 0.05), compared with the ALI group (all <em>P</em> &lt; 0.001). TAF obviously reversed effects of ALI modeling, and remarkably downregulated the expression of PERK and upregulated Nrf2 (all <em>P</em> &lt; 0.001) compared with the ALI rats. In conclusion, TAF attenuates alcohol-induced livery injury through suppressing Keap-1/Nrf2/HO-1, NF-κB/MAPK and PERK/Nrf2 signaling pathways mediated oxidative stress and inflammation in ALI rats.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102913"},"PeriodicalIF":2.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911874","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":"Mechanism of EZH2-mediated histone methylation promoting bFGF-induced angiogenesis of human umbilical vein endothelial cells","authors":"Min Gao ,&nbsp;Chen Xing","doi":"10.1016/j.tice.2025.102945","DOIUrl":"10.1016/j.tice.2025.102945","url":null,"abstract":"<div><div>This study aims to explore the role of enhancer of zeste homolog 2 (EZH2)-mediated histone methylation in basic fibroblast growth factor (bFGF)-induced angiogenesis of human umbilical vein endothelial cells (HUVECs). EZH2, vascular endothelial growth factor A (VEGFA), miR-340–5p, and nuclear factor-erythroid 2-related factor 2 (NRF2) expressions in bFGF-induced HUVECs were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. After transfection of EZH2 siRNA, NRF2 siRNA, or miR-340–5p inhibitor, cell migration and angiopoiesis were assessed by Transwell and tube formation assays. Chromatin immunoprecipitation (ChIP) was performed to analyze the enrichment of EZH2 or trimethylated H3 lysine 27 (H3K27me3) on NRF2 promoter. The binding between NRF2 and miR-340–5p was verified by ChIP and dual-luciferase assay. EZH2 was highly expressed while miR-340–5p and NRF2 were poorly expressed in bFGF-induced HUVECs. Silence of EZH2 restrained HUVEC migration, and reduced the number of branches and tube length. Mechanically, EZH2 enhances the enrichment of H3K27me3 on the NRF2 promoter, thereby repressing NRF2 expression and further leading to transcriptional repression of miR-340–5p. In conclusion, EZH2 inhibits the NRF2/miR-340–5p axis and promotes bFGF-induced angiogenesis of HUVECs by increasing the H3K27me3 modification on the NRF2 promoter.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 102945"},"PeriodicalIF":2.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918516","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":"Pro-apoptotic and mitochondria-disrupting effects of 4-methylthiazole in K562 leukemia cells: A mechanistic investigation","authors":"Neslihan Meriç ,&nbsp;Ezgi Kar ,&nbsp;Fatih Kar","doi":"10.1016/j.tice.2025.102937","DOIUrl":"10.1016/j.tice.2025.102937","url":null,"abstract":"<div><div>Thiazole derivatives have garnered attention for their anticancer potential. This study investigates the antileukemic effects of 4-methylthiazole on K562 chronic myeloid leukemia (CML) cells, focusing on apoptosis induction and mitochondrial dysfunction. Cell viability was assessed using MTS assays; apoptosis and necrosis were analyzed via Annexin V/PI staining and flow cytometry; mitochondrial membrane potential changes were evaluated with JC-1 dye; gene expression levels were measured by qRT-PCR; and levels of apoptosis- and cytokine-related proteins were quantified using ELISA. Treatment with 4-methylthiazole led to selective cytotoxicity in K562 cells while sparing healthy peripheral blood mononuclear cells (PBMNCs). Apoptotic induction was evidenced by Caspase-3 (CASP-3) activation, Cytochrome-C (CYT-C), release, and mitochondrial depolarization. Gene expression analysis showed upregulation of pro-apoptotic markers such as <em>TP53</em> (tumor suppressor protein 53), <em>BAX</em> and <em>BAK</em> (pro-apoptotic Bcl-2 family proteins), while upregulation of <em>CASP3</em> (caspase-3) expression was not statistically significant. Conversely, levels of <em>GPX4</em> (glutathione peroxidase 4, involved in oxidative stress protection) remained unchanged, indicating an apoptosis mechanism independent of oxidative stress. Additionally, <em>SEMA3A</em> (Semaphorin 3 A, involved in tumor progression and cell signaling) was significantly downregulated. Cytokine profiling revealed a dose-dependent modulation of IL-6, while TNF-α and IL-10 levels remained unaffected. These findings suggest that 4-methylthiazole induces apoptosis through mitochondrial pathways, affects cytokine signaling, and selectively targets leukemia cells, supporting its potential as a therapeutic candidate for CML treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102937"},"PeriodicalIF":2.7,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890561","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":"Resveratrol protects against letrozole-induced renal damage in a rat model of polycystic ovary syndrome: A biochemical, histological, and immunohistochemical study","authors":"Einas M. Yousef ,&nbsp;Samar M. Abd El-moneam ,&nbsp;Shimaa Mohammad Yousof ,&nbsp;Safaa Abdallah Mohammed ,&nbsp;Basma Osman Sultan ,&nbsp;Basma S.A. Mansour","doi":"10.1016/j.tice.2025.102934","DOIUrl":"10.1016/j.tice.2025.102934","url":null,"abstract":"<div><h3>Background</h3><div>Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects 9–18 % of women, often associated with metabolic and renal complications. This study aimed to investigate the renoprotective effects of resveratrol (RSV) in a letrozole-induced rat model of PCOS, focusing on biochemical, histological, ultrastructural, and immunohistochemical alterations.</div></div><div><h3>Methods</h3><div>Thirty female rats were randomly divided into five groups: negative control, only RSV-treated, PCOS-induced (sham), metformin-treated, and RSV-treated. Serum testosterone, urea, and creatinine levels were assessed. Renal tissues underwent histological, immunohistochemical, ultrastructural, and morphometric analyses. Additionally, TGF-β1 mRNA expression was evaluated using qRT-PCR.</div></div><div><h3>Results</h3><div>Letrozole administration significantly elevated serum testosterone, urea, and creatinine levels, indicating PCOS-associated renal dysfunction. Histological and ultrastructural analysis revealed severe glomerular and tubular alterations in the sham group. The administration of RSV significantly restored renal architecture and function more effectively than metformin. Immunohistochemistry analysis showed that RSV reduced Proliferating Cell Nuclear Antigen (PCNA) overexpression and restored B-cell Lymphoma 2 (BCL-2) expression, suggesting a protective effect against cellular stress and apoptosis. Moreover, RSV significantly downregulated TGF-β1 expression, indicating its anti-fibrotic and anti-inflammatory role in PCOS-related renal damage.</div></div><div><h3>Conclusion</h3><div>In a PCOS rat model, RSV protects effectively against letrozole-induced structural and functional renal damage. It demonstrates superior efficacy over metformin in restoring renal function, reducing apoptosis, and mitigating fibrosis. These findings suggest that RSV may serve as a potential adjunct therapy for preventing PCOS-associated renal complications, emphasizing the need for further investigations.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102934"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890682","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":"Modulation of TLR4 mediated HMGB1/RAGE/NF-κB axis through linarin against fenvalerate provoked cardiotoxicity","authors":"Fuad M. Alzahrani ,&nbsp;Arifa Mehreen ,&nbsp;Qurat Ul Ain ,&nbsp;Adnan Ali ,&nbsp;Khalid J. Alzahrani ,&nbsp;Khalaf F. Alsharif","doi":"10.1016/j.tice.2025.102931","DOIUrl":"10.1016/j.tice.2025.102931","url":null,"abstract":"<div><div>Fenvalerate (FVN) is a potent insecticidal agent that exhibits a wide range of organ impairments including cardiac damage. Linarin (LIN) is a polyphenolic compound with a diverse range of pharmacological potentials. The present investigation was conducted to quantify the mitigative ability of LIN against FVN induced cardiotoxicity. Thirty-six male Sprague Dawley rats were divided into four groups i.e., the control, FVN (40 mg/kg), FVN (40 mg/kg) + LIN (50 mg/kg) and LIN (50 mg/kg) alone treated group. It was observed that FVN exposure exacerbated the gene expression of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), receptor for advanced glycation end products (RAGE), interleukin-1β (IL-1β), high mobility group box 1 (HMGB1), cyclooxygenase-2 (COX-2), nuclear factor- kappa B (NF-κB), toll-like receptor 4 (TLR4), and tumor necrosis factor-α (TNF-α). Moreover, the levels of reactive oxygen species (ROS) &amp; malondialdehyde (MDA) were surged-up while the enzymatic action of heme oxygenase-1 (HO-1), glutathione (GSH), glutathione Peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GSR), and catalase (CAT) were decreased following the FVN intoxication. Besides, FVN administration upregulated the concentrations of troponin-I, troponin-T, c-reactive protein, creatine kinase-MB (CK-MB), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) in cardiac tissues. FVN exposure increased the levels of Caspase-9, Bax and Caspase-3 while reducing the levels of Bcl-2. Cardiac tissues showed abnormal morphology after FVN intoxication. Nonetheless, LIN therapy remarkably alleviated cardiac damages instigated through FVN exposure due to its anti-inflammatory, anti-oxidative as well as anti-apoptotic potentials.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102931"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890557","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":"Mechanism of the effect of Juan-Tong-Yin on endoplasmic reticulum stress-autophagy in endometriosis rats based on protein kinase R-like endoplasmic reticulum kinase/eukaryotic cell initiation factor 2α pathway","authors":"Qi-Yu Liu ,&nbsp;Jing Li ,&nbsp;Feng-Qun Gu ,&nbsp;Feng-Yun Meng ,&nbsp;Ying Liu ,&nbsp;Wei-Hong Li","doi":"10.1016/j.tice.2025.102935","DOIUrl":"10.1016/j.tice.2025.102935","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the mechanism of Juan-Tong-Yin (JTY) on endoplasmic reticulum (ER) stress-autophagy in endometriosis (EM) rats through the protein kinase R-like endoplasmic reticulum kinase (PERK)/eukaryotic cell initiation factor 2α (eIF2α) autophagy pathway.</div></div><div><h3>Methods</h3><div>An EM rat model was established. A total of 70 Sprague–Dawley (SD) rats were randomly divided into the normal control group, model group, JTY high-, medium- and low-dose groups (25.4, 12.7, and 6.35 g/kg, respectively), progesterone group (0.26 mg/kg), and ER stress group (2-DG, 100 mg/kg). The seven groups were given the corresponding dose of the drug through gavage in the administration group and saline through gavage (1 mL/100 g) in the model and normal control groups. The drugs were administered continuously for 4 weeks. Ectopic lesion volume and pelvic adhesion score were measured. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of ectopic endothelium in rats. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum inflammatory marker C-reactive protein (CRP) and estradiol (E2) in each group; immunohistochemistry, real-time fluorescence quantitative polymerase chain reaction (Real-time PCR), and protein immunoblotting method (Western blotting) were used to detect the expressions of ectopic endothelial PERK, eIF2α, and microtubule-associated protein light chain 3B (LC3B) and mRNA.</div></div><div><h3>Results</h3><div>Compared with the model group, the JTY-treated rats exhibited significantly reduced ectopic lesion volume (P &lt; 0.05), the pelvic adhesion score was decreased (<em>P</em> &lt; 0.05), and the pathology of the ectopic endothelium showed varying degrees of atrophy, detachment, and gland reduction. In addition, serum inflammatory marker CRP and E2 levels were decreased significantly, and JTY promoted the expression of PERK, eIF2α, and microtubule-associated protein LC3B protein and mRNA (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>JTY ameliorates EM by activating the PERK/eIF2a pathway, enhancing cell ER stress and autophagy, improving the inflammatory microenvironment, and ultimately mitigating EM in rats.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102935"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890556","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":"Ferroptosis targeting offers a therapeutic target for septic cardiomyopathy","authors":"Pengsi Zhou,&nbsp;Mengxue Liu,&nbsp;Tao Lv","doi":"10.1016/j.tice.2025.102930","DOIUrl":"10.1016/j.tice.2025.102930","url":null,"abstract":"<div><div>Sepsis-induced cardiac dysfunction, usually termed sepsis-induced cardiomyopathy or septic cardiomyopathy(SCM), is developed in approximately 70 % of the patients with sepsis, making it is a major concern for sepsis patients. However, the pathogenesis of SCM remain incompletely understood. Ferroptosis, a newly identified mechanism of regulated cell death, characterized by a decline in antioxidant capacity, iron accumulation, and lipid peroxidation(LPO), is involved in sepsis and SCM. Moreover, ferroptosis inhibitors confer a novel therapeutic regimen in SCM. In this Review, we first summarizes the core mechanism of ferroptosis, with an emphasis on how best to interpret ferroptosis leads to the genesis of SCM. We then highlights our focus on the emerging different types of therapeutic ferroptosis inhibitors and summarizes their pharmacological beneficial effect to treat SCM. This review highlights a novel potential therapeutic strategy for SCM by pharmacologically inhibiting ferroptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"Article 102930"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874831","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}