Molecular and Cellular Biochemistry最新文献

{"title":"Inhibition of endothelial S1PR2 preserves blood-brain barrier integrity after traumatic brain injury through activating the PI3K-AKT signaling pathway.","authors":"Hongbo Cheng, Qin Wang, Yijiao Men, Yaqing An, Botao Ma, Shimei Dai, Zhuang Jing, Xuerui He, Xiaoqing Bao, Yinbo Long, Jiegang Yu, Yang Wu, Guozhu Sun","doi":"10.1007/s11010-026-05546-6","DOIUrl":"https://doi.org/10.1007/s11010-026-05546-6","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is a major cause of blood-brain barrier (BBB) disruption and neurological dysfunction, wherein endothelial dysfunction plays a critical pathogenic role. As a member of the G protein-coupled receptor family, sphingosine-1-phosphate receptor 2 (S1PR2) is known to regulate vascular homeostasis; however, its specific role in protecting the blood-brain barrier following TBI remains unclear. This study aims to elucidate the mechanism by which S1PR2 maintains blood-brain barrier integrity and to evaluate the therapeutic potential of S1PR2 inhibition after TBI. A mouse model of TBI was established using controlled cortical impact, while human umbilical vein endothelial cells (HUVECs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemia-reperfusion injury in vitro. We employed shRNA technology to knock down S1PR2 expression and utilized single-cell RNA sequencing (dataset GSE269748) to characterize cell type-specific expression profiles. Endothelial function, blood-brain barrier permeability, inflammatory responses, and cell apoptosis were assessed using tube formation assays, transendothelial electrical resistance (TER) analysis, Western blotting, immunofluorescence, qPCR, ELISA, Evans blue staining, and brain water content measurements. Behavioral tests including open field test and novel object recognition test were used to evaluate the recovery of neurological function. At the same time, the PI3K-AKT pathway was interfered by S1PR2 knockdown mediated by AAV virus and pharmacological inhibitor (JTE-013/LY94002) or activator (Cyn). Single-cell analysis revealed that S1PR2 is specifically expressed in endothelial cells and is significantly upregulated following TBI. In vitro, S1PR2 knockdown counteracted the OGD/R-induced reduction in tube formation capacity and the elevation in transendothelial electrical resistance, and restored the expression of tight junction proteins Occludin and ZO-1. RNA-seq and KEGG enrichment analysis suggested that PI3K-AKT pathway was the key downstream target of S1PR2. In vivo experiments demonstrated that S1PR2 expression peaked at 72 h post-TBI and colocalized with CD31, while the ratios of p-PI3K/PI3K and p-AKT/AKT were markedly reduced. Intervention targeting S1PR2 significantly enhanced locomotor activity and novel object recognition, reduced brain lesion area, suppressed neuronal apoptosis and inflammatory cytokine levels, and restored BBB integrity in TBI mice. Mechanismally, activation of PI3K-AKT pathway could mimic the protective effect of S1PR2 knockdown, whereas inhibition of this pathway negated the improvements in BBB integrity and neurological function induced by S1PR2 knockdown. Endothelial S1PR2 is a critical regulator of vascular homeostasis after TBI. Inhibition of Endothelial S1PR2 preserves blood-brain barrier integrity, mitigates neuroinflammation and apoptosis, and promotes neurological recovery through activation of the PI3K-AKT signali","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidptosis-related gene DSTN predicts prognosis and promotes malignant progression in head and neck squamous cell carcinoma.","authors":"Xingzhi Peng, Likang Chen, Jing Zhang, Lifang Yang, Xia Wu","doi":"10.1007/s11010-026-05559-1","DOIUrl":"https://doi.org/10.1007/s11010-026-05559-1","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) is the most common malignant tumor of the head and neck tissues. Disulfidptosis is a novel form of programmed cell death caused by disulfide stress, which mainly manifests as cytoskeleton protein and F-actin breakdown. In this study, we collected 504 HNSCC patients' data from The Cancer Genome Atlas (TCGA) database and constructed a prognostic disulfidptosis-related gene signature for HNSCC patients. Destrin (DSTN), an actin depolymerizing factor, was considered a reliable prognostic biomarker, with its high expression significantly associated with shorter overall survival (OS) and progression-free survival (PFS). Functional enrichment analysis revealed that DSTN was positively correlated with extracellular matrix (ECM)-related genes, and particularly enriched in ECM degradation pathways and matrix metalloproteinase (MMP) family members, such as MMP10 and MMP3. qPCR and Western blot results showed that knockdown of DSTN inhibited the expression of ECM-related genes MMP10 and MMP3 in HNSCC cells. Tumor immune microenvironment analysis revealed that DSTN was negatively correlated with infiltration levels of various immune cells, immune checkpoints, and tumor mutational burden (TMB). Co-culture experiment of H9 cells with HNSCC cells further demonstrated that DSTN knockdown significantly upregulated the CD274 expression in HNSCC cells. In vitro functional experiments showed that DSTN knockdown effectively inhibited HNSCC cell proliferation and migration, suppressed glucose metabolism, and blocked Wnt/β-catenin signaling pathway activation; additionally, it induced F-actin contraction, triggering disulfidptosis. In vivo xenograft experiments confirmed that DSTN knockdown significantly inhibited HNSCC tumor growth. In conclusion, this study demonstrates that DSTN is a key driver promoting the malignant progression of HNSCC; high DSTN expression indicates poor prognosis, while its downregulation exerts tumor-suppressive effects through multiple mechanisms, including inhibiting the secretion of MMPs, suppressing glucose metabolism, blocking the Wnt/β-catenin signaling pathway, and inducing disulfidptosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transplantation of Ru265-treated mitochondria enhances the therapeutic impact on skeletal muscle ischemia-reperfusion injury.","authors":"Saima Barki, Fazal Wahid, Shafia Khan, Laiba Tariq Abbasi, Zarrish Rubab, Ameer Hamza, Farman Ullah, Khadeeja Ahsan, Durre Shehwar, Muhammad Rizwan Alam","doi":"10.1007/s11010-026-05563-5","DOIUrl":"https://doi.org/10.1007/s11010-026-05563-5","url":null,"abstract":"<p><p>Mitochondrial transplantation (MT) is a promising therapeutic approach for the treatment of several pathologies, including ischemia-reperfusion injury (IRI). However, its efficacy remains limited by the high calcium concentration of the transplantation milieu. Elevated extracellular calcium induces MCU-mediated matrix calcium overload, leading to the opening of the permeability transition pore and metabolic collapse of the transplanted organelles. We hypothesized that shielding mitochondria from the adverse effects of high calcium using the reversible MCU inhibitor, Ru265, would increase the efficacy of MT therapy. An acute, non-invasive hindlimb skeletal muscle IRI model was established in BALB/c mice using orthodontic rubber bands to mimic peripheral artery disease. Isolated liver mitochondria were treated with Ru265 and evaluated for their responsiveness to calcium using the mitochondrial swelling assay. Mice subjected to hindlimb IRI received either standard MT (Mitochondria alone) or Ru265-treated mitochondria (Mito + Ru), and treatment efficacy was evaluated using various parameters. IRI induced significant changes in mouse body weight, musculoskeletal dysfunction, systemic inflammation, lipid peroxidation, and skeletal muscle damage. While standard MT therapy provided baseline recovery, the Mito + Ru group demonstrated superior outcomes, including significant body weight recovery, reduced infarct size, and attenuated oxidative stress. Thus, reversible shielding of exogenous mitochondria from calcium stress using Ru265 enhances the efficacy of MT therapy in rodent skeletal muscle IRI.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polarized mitochondrial respiratory chain complexes in synaptic mitochondria induced by plasticity signals.","authors":"Xi Wang, Gang Zhou, Yi Hu, Kaiyuan Liu, Chong Zuo, Tingting Yan, Ji-Song Guan, Hong Xie","doi":"10.1007/s11010-026-05562-6","DOIUrl":"https://doi.org/10.1007/s11010-026-05562-6","url":null,"abstract":"<p><p>Mitochondria are well established as key supporters of synaptic plasticity, yet the nanoscale spatial distribution of specific mitochondrial membrane proteins during this process remains poorly understood. Using 3D MINFLUX nanoscopy, we investigated their polarized distribution within synapses of cortical neurons undergoing chemical long-term potentiation (cLTP). Upon cLTP induction in DIV17 neurons, we observed an increased mitochondrial occupancy in stimulated synapses. Respiratory complexes of the inner mitochondrial membrane (IMM)-such as COX-IV and SDHA-showed a polarized accumulation near presynaptic sites, as validated by cluster analysis and 3D mapping. By contrast, outer mitochondrial membrane (OMM) proteins, including TOMM20 and VDAC, exhibited no significant polarized distribution. Together, these results demonstrate that cLTP selectively remodels the inner mitochondrial membrane to address localized energy requirements, highlighting the power of 3D MINFLUX for resolving protein organization with subcellular precision.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the off-label use of liraglutide in the treatment of obesity: a review.","authors":"Carla Bruna Amorim Braga, João Paulo Viana Araújo Segundo, Carlos Alberto Alves Dias Filho","doi":"10.1007/s11010-026-05560-8","DOIUrl":"https://doi.org/10.1007/s11010-026-05560-8","url":null,"abstract":"<p><p>Liraglutide, a glucagon-like peptide-1 (GLP-1) analog, has been used off-label for the treatment of obesity due to its considerable weight-reducing effects. This integrative review evaluated experimental studies in humans in order to explore the pharmacological mechanisms, metabolic effects, and the various clinical responses involved in the use of this drug. The research was conducted in the PubMed database, considering articles written in English and published in the last 10 years, with 9 studies included. The studies demonstrated that liraglutide is effective for weight loss and acts through gastric emptying, modulation of satiety, and influences on brain regions. Additionally, genetic polymorphisms may interfere with the clinical response. Regarding metabolic effects, improvements in glycemia and hepatic steatosis were observed, as well as possible anti-inflammatory action and improvement in blood pressure and lipid profile. The efficacy of liraglutide does not depend on variables such as BMI (Body Mass Index) or age; however, alcohol consumption and proper adherence to treatment may influence clinical outcomes. The main adverse effects, such as nausea and constipation, were well tolerated. Therefore, liraglutide can be considered a promising alternative in the management of obesity, especially in populations with multiple metabolic risk factors.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated placental inflammation as a mediator of adverse outcomes in gestational diabetes mellitus.","authors":"Shweta Madiwale, Aditi Godhamgaonkar, Aishwarya Karkhanis, Vaishali Kasture, Hemlata Pisal, Karuna Randhir, Deepali Sundrani, Girija Wagh, Sanjay Gupte, Sadhana Joshi","doi":"10.1007/s11010-026-05561-7","DOIUrl":"https://doi.org/10.1007/s11010-026-05561-7","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) is a prevalent pregnancy complication associated with adverse maternal and neonatal outcomes. This study aims to investigate the expression of key inflammatory markers - tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-6 (IL-6), and nuclear-factor kappa-light chain of B (NFκB) in the placental tissue of GDM and non-GDM women. Additionally, the study explores associations between these markers and neonatal characteristics, placental dimensions, and resolvins levels. This cross-sectional study included 416 singleton pregnant women, comprising 209 with GDM and 207 non-GDM. Placental protein and mRNA expression levels of TNF-α, IL-10, IL-6, and NFκB were measured using ELISA and RT-qPCR. Associations between resolvins and inflammatory markers were also assessed. Placental protein levels of TNF-α, IL-10, and NFκB, as well as gene expression levels of IL-6, were elevated in the GDM group. Furthermore, TNF-α was negatively associated with major axis, thickness and center and cord insertion. Inflammatory markers were negatively associated with head circumference at birth. A negative association was found between placental resolvin E1 (RvE1) levels and the inflammatory markers IL-10, NFκB, and TNF-α. The study highlights the association between pro-inflammatory and pro-resolving mediators in the placenta, providing insights into GDM and its adverse outcomes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A cardiac fibrosis specific circRNA_006640 sponges miR-7648-3p and miR-185-3p to synergistically up-regulate CTGF.","authors":"Lijuan Yang, XiaoMin He, Kai Luo, Xinjie Zhang, Haoyu Li, Wenjun Zhou, Jinwen Pang, Mengyi Zhang, Zijie Zhou, Min Ren","doi":"10.1007/s11010-026-05547-5","DOIUrl":"https://doi.org/10.1007/s11010-026-05547-5","url":null,"abstract":"<p><p>Cardiac fibrosis is a critical pathological feature in nearly all forms of heart disease and contributes to heart failure. However, existing diagnostic and therapeutic approaches are insufficient for detecting fibrosis or targeting conventional pathways. Further molecular investigations are urgently needed to develop effective treatments. Circular RNAs (circRNAs), distinguished by their stability and regulatory roles, show significant potential. CircRNA_006640 was substantially upregulated in left ventricular tissues of male mice subjected to transverse aortic constriction, as well as in blood samples. Gain- and loss-of-function studies confirmed that circRNA_006640 promoted proliferation and phenotypic transformation in mouse cardiac fibroblasts. Real-time quantitative reverse transcription polymerase chain reaction and Western blotting demonstrated that circRNA_006640 suppressed miR-7648-3p and miR-185-3p, which in turn inhibited connective tissue growth factor (CTGF). Furthermore, there was a synergistic effect between miR-7648-3p and miR-185-3p to enhance the suppression of CTGF. In vivo, circRNA_006640 markedly exacerbated cardiac fibrosis. Knockdown of circRNA_006640 using small interfering RNA effectively mitigated cardiac fibrosis and preserved cardiac function, indicating therapeutic potential for antifibrotic strategies. CircRNA_006640 acts as a novel upstream regulator of CTGF, exacerbating cardiac fibrosis by sponging miR-7648-3p and miR-185-3p. The synergistic interaction between miR-7648-3p and miR-185-3p strengthens the profibrotic effect. Targeting CircRNA_006640 may hold promising therapeutic potential for cardiac fibrosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the pro-inflammatory mechanism mediated by the RANK-SPP1 axis in macrophage immunomodulation during atherosclerosis.","authors":"Qiyu Sun, Yanbo Hu, Zeming Sun, Mingyan Shang, Zhengyi Li, Juan Shen, Zhenzhen Cui, Jiaxin Yang, Xiaowen Ma, Min Li","doi":"10.1007/s11010-026-05554-6","DOIUrl":"https://doi.org/10.1007/s11010-026-05554-6","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic inflammatory disease driven by macrophages. While the RANK/RANKL signaling axis and SPP1 (osteopontin) are individually known to contribute to vascular inflammation, whether they function within a coordinated regulatory hierarchy in plaque macrophages remains unknown. This study investigates whether RANK defines a pro-inflammatory macrophage subset and whether SPP1 acts as a critical downstream effector within the RANK signaling pathway to promote AS progression. Plaque tissue samples were obtained from databases of atherosclerotic patients, experimental atherosclerotic animal models, and in vitro cell experiments to analyze the role of the RANK molecule and macrophages in atherosclerosis and to investigate its association with disease severity. Single-cell RNA sequencing, histological analysis, co-culture of ox-LDL with macrophages, and gene knockout animal experiments were employed to study the mechanism of RANK high expression on macrophages in atherosclerosis progression. We found that high expression of RANK is closely correlated with the severity of atherosclerosis. Single-cell transcriptomic analysis revealed that RANK⁺ cells are primarily enriched in macrophages, and RANK⁺ macrophages exhibit active metabolic and immune response pathways in AS. Cell communication analysis showed that RANK⁺ macrophages are closely associated with SPP1, with SPP1 being a key gene in RANK⁺ macrophages. Furthermore, the number of RANK⁺/SPP1⁺ macrophages increases with AS progression. Mechanistically, SPP1 is a downstream gene of RANK. RANK promotes AS progression by upregulating SPP1, acting through macrophage immunomodulatory pathways. Knocking out RANK in macrophages suppressed SPP1 expression and inhibited the ability of macrophages to phagocytose ox-LDL. Additionally, inhibiting RANK in mouse and rat AS models similarly suppressed SPP1 expression and reduced plaque formation, thereby delaying AS progression. This study establishes a previously unrecognized RANK-SPP1 signaling axis that functions as a macrophage-autonomous inflammatory amplifier in atherosclerosis. We demonstrate that RANK defines a distinct pro-inflammatory macrophage subset characterized by high metabolic and inflammatory pathway activity. Mechanistically, RANK transcriptionally upregulates SPP1 via the NF-κB pathway, and the accumulation of RANK⁺SPP1⁺ macrophages correlates with disease severity. Pharmacological inhibition of RANK signaling attenuates plaque progression in preclinical models, highlighting this axis as a potential therapeutic target for AS.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Co-translational profiling in the cardiac endothelium in response to LPS-induced inflammation in female mice in vivo: a proof-of-concept approach.","authors":"Chad M Warren, Bhairavi Swaminathan, Paulina Langa, Stephanie R Villa, Walter C Thompson, Magdalena Chrzanowska, Jan K Kitajewski, R John Solaro, Beata M Wolska, Paul H Goldspink","doi":"10.1007/s11010-026-05551-9","DOIUrl":"https://doi.org/10.1007/s11010-026-05551-9","url":null,"abstract":"<p><p>Producing functional proteins involves multiple steps during mRNA translation on the ribosomes. However, co-translational regulatory mechanisms remain poorly characterized in intact mammalian systems. As a proof-of-concept, we developed a multi-omics approach to investigate endothelial-specific, co-translational regulation by modifying the translating ribosome affinity purification (TRAP) in vivo. We simultaneously co-immunoprecipitated (IP) polysome-associated mRNAs and proteins from the hearts of hemagglutinin-tagged ribosomal protein L22 mice (RiboTag) crossed with inducible endothelial-specific Cdh5CreERT2 mice (RiboTag_EC). To perturb endothelial function, female mice were injected with E. coli lipopolysaccharide (LPS) (6 mg/Kg, i.p., 12 h). Hearts were homogenized, with ~ 10% used for input RNA-Seq and proteomics controls, and the remainder for IP of ribosome-bound polyadenylated mRNA and proteins. Endothelial cell transcripts (pecam1, cdh5) were enriched > 5-fold, while markers characteristic of other cell types were significantly depleted (< 0.05 q-value). We aligned transcriptomic and proteomic datasets (> 1250 overlapping terms) to identify pathways associated with concordant and discordant co-translational regulation. LPS was identified as the upstream regulator of the co-translational dataset that was concordantly regulated. Upregulated mRNAs but not proteins related to glycolysis were discordantly regulated. These findings validate our proof-of-concept multi-omics approach as a predictive platform for identifying disease-relevant pathways regulated at the co-translational level in vivo.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Bidens pilosa extract Jacein alleviates hypertension by restoring mitochondrial dynamic balance through modulating the FAM210A/OPA1 signaling pathway.","authors":"Tao Yang, Xiaoxiao Lu, Qi Chen","doi":"10.1007/s11010-026-05537-7","DOIUrl":"https://doi.org/10.1007/s11010-026-05537-7","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}