Molecular and Cellular Biochemistry最新文献

{"title":"NDRG1-PTEN association modulates PTEN C-terminal tail phosphorylation in insulin-resistant neurons.","authors":"Atreyi Mukherjee, Shankari Prasad Datta, Chinmoy Sankar Dey","doi":"10.1007/s11010-026-05764-y","DOIUrl":"https://doi.org/10.1007/s11010-026-05764-y","url":null,"abstract":"<p><p>N-myc Downstream Regulated Gene-1 (NDRG1), implicated in the regulation of the PI3K-Akt pathway, regulates the expression of Phosphatase and TENsin homolog (PTEN), a key insulin signaling regulator. However, NDRG1's role in the insulin signaling pathway is not understood. This study aimed to clarify whether and how NDRG1 regulates PTEN C-terminal phosphorylation at residues S380/T382/T383 in the context of neuronal insulin signaling and resistance. It was found that NDRG1 associates with PTEN and regulates its phosphorylation at residues S380/T382/T383 in mouse hippocampal neurons. Co-immunoprecipitation and immunofluorescence microscopy indicated that pairwise associations between NDRG1-PTEN and Protein Phosphatase 2A (PP2A)-PTEN are upregulated by insulin stimulation and are further augmented in insulin-resistance. Deletion of the NDRG1 C-terminal region markedly reduced detectable PTEN co-immunoprecipitation, suggesting a role for this region in NDRG1-PTEN association. Silencing NDRG1 increased PTEN C-terminal phosphorylation at residues S380/T382/T383. Additionally, data from PP2A-specific inhibitor and siRNA support the involvement of PP2A in PTEN C-terminal dephosphorylation. We also utilized a phospho-dead NDRG1 mutant to demonstrate that phosphorylation of NDRG1 at T346 plays a role in the modulation of PTEN C-terminal phosphorylation. Thus, our results suggest that NDRG1 modulates PTEN C-terminal phosphorylation at residues S380/T382/T383 in neuronal cells and neuronal insulin-resistance affects this regulation by NDRG1.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183288","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":"Piperine enhances hyperthermia-induced apoptosis in AGS gastric cancer cells by increasing reactive oxygen species and attenuating heat-shock protein induction.","authors":"Chae Ryeong Ahn, Min Gyu Shin, In-Seung Lee, Jinbong Park, Jai-Eun Kim, In Jin Ha, Kwang Seok Ahn, Seung Ho Baek","doi":"10.1007/s11010-026-05757-x","DOIUrl":"https://doi.org/10.1007/s11010-026-05757-x","url":null,"abstract":"<p><p>Thermotherapy can potentiate anticancer activity, yet heat-induced stress adaptation-largely involving the HSF1-HSP axis-may limit its efficacy. Here, we investigated whether piperine acts as a thermosensitizer in AGS gastric cancer cells and explored associations with oxidative stress, apoptosis, and the heat-shock response. AGS cells were treated with piperine and subjected to mild hyperthermia (43 °C), followed by evaluation of viability, migration, colony formation, apoptosis, and cell-cycle distribution. Piperine enhanced hyperthermia-induced growth suppression, reduced scratch closure, and increased apoptotic cell death, accompanied by an increase in the sub-G1 populations. The combination elevated intracellular ROS, promoted caspase activation, and was associated with attenuation of pro-survival signaling. Piperine attenuated hyperthermia-induced HSP expression, most prominently HSP27 and HSP90, without reducing HSF1 or its activating phosphorylation. To extend these observations, we validated the cytotoxic and apoptotic phenotype in a second gastric cancer cell line, NCI-N87: piperine plus hyperthermia increased cleaved caspase-3, and NAC pretreatment partially attenuated this increase, supporting a contribution of oxidative stress to the apoptotic response, whereas the heat-shock protein response in NCI-N87 cells was not uniformly reproduced, indicating a cell-line-dependent pattern. Collectively, piperine enhanced hyperthermia-associated cytotoxicity and apoptosis in both gastric cancer cell models, whereas attenuation of HSP expression was more evident in AGS cells and was not uniformly reproduced in NCI-N87 cells, supporting further study as an adjunct strategy for hyperthermia-based anticancer approaches.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183233","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":"Exercise improves heart failure by regulating cardiomyocyte autophagy via the ILF3/lncRNA NEAT1 axis.","authors":"Ying Zhang, Rui Song, Ying Zhao","doi":"10.1007/s11010-026-05772-y","DOIUrl":"https://doi.org/10.1007/s11010-026-05772-y","url":null,"abstract":"<p><p>Heart failure (HF) is a common cardiovascular disease. It has been reported that the lncRNA NEAT1 is involved in the progression of HF and that exercise can regulate the expression of NEAT1 in muscle tissue. This study aimed to investigate whether exercise can influence HF progression by regulating NEAT1 expression and to elucidate its molecular mechanisms. Two independent rat HF models were established separately by intraperitoneal injection of isoproterenol hydrochloride (ISO) or by abdominal aortic constriction (AAC), whereas an in vitro HF model was induced by angiotensin II (Ang-II) in rat H9c2 cardiomyocytes. After 4 weeks of exercise training, serum NT-pro BNP levels were measured in the rats, and cardiac injury was assessed via HE staining and Masson staining. The expression of key genes and proteins was detected using RT‒qPCR, Western blotting, and immunofluorescence, and apoptosis was evaluated via TUNEL staining. RNA immunoprecipitation experiments were performed to validate the interaction between NEAT1 and ILF3. NEAT1 expression is upregulated in HF, and its knockdown can inhibit cellular damage in in vitro and in vivo HF models and improve cardiac function in rats. Additionally, exercise training reduces the expression of NEAT1 in the cardiac tissues of HF rats, and overexpression of NEAT1 weakens the inhibitory effect of exercise training on the progression of HF in rats, indicating that exercise training improves HF progression by suppressing NEAT1 expression. Mechanistic studies revealed that upregulated ILF3 in HF binds to NEAT1 to stabilize its expression, thereby activating the PI3K/AKT/mTOR signaling pathway, which subsequently inhibits autophagy, ultimately leading to HF. Exercise training can downregulate NEAT1 expression, thereby suppressing abnormal activation of the PI3K/AKT/mTOR signaling pathway and further relieving HF progression through the activation of autophagy. Additionally, NEAT1 expression is regulated by ILF3.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183156","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":"SMAD3 phosphorylation inhibitor, tomentosenol A arrests cell cycle progression and induces apoptotic signalling in cultured fibroblasts: implications for anti-scarring activity.","authors":"Lisa J Randall, Trong D Tran, Georgia Siddals, Robert J Harvey, Annabelle Greensill, Kate E Woodhill, Fraser D Russell","doi":"10.1007/s11010-026-05771-z","DOIUrl":"https://doi.org/10.1007/s11010-026-05771-z","url":null,"abstract":"<p><p>Hypertrophic scars are characterised by excessive fibroblast proliferation, myofibroblast activation, aberrant extracellular matrix deposition and reduced apoptosis. Current anti-scar therapies have variable efficacy and are limited by recurrence, tissue damage and pain, so new strategies are needed. In this study, we examined the efficacy of tomentosenol A, a meroterpenoid compound isolated from Australian stingless bee propolis, to intervene in the development of the cellular hallmarks of scar tissue. The effects of tomentosenol A were compared to two structural analogues (4S)- and (4R)-ficifolidione, using cultured HEK293 cells expressing a SMAD binding element/secreted embryonic alkaline phosphatase reporter and cultured normal adult human dermal fibroblasts. Cell cycle progression was assessed by CDK2 (Tyr15) and Histone H3 (Ser10) phosphorylation, apoptotic signalling by caspase-3/7 activity, and fibroblast wound closure by live-cell scratch-wound assay. The findings revealed that all compounds inhibited TGF-β1-stimulated fibroblast activation, as evidenced by prevention of α-smooth muscle actin assembly in cytoskeletal microfilaments, but only tomentosenol A prevented TGF-β1-stimulated SMAD signalling and fibronectin secretion. Tomentosenol A stimulated G1/S transition and arrested cells at G2/M; (4S)-ficifolidione was without effect on cell cycle progression while (4R)-ficifolidione arrested cells at G1/S. Only tomentosenol A stimulated caspase-3/7 activity, and this effect was attenuated by TGF-β1. Tomentosenol A also concentration-dependently slowed fibroblast wound closure. The findings establish tomentosenol A as a lead compound to test for anti-scarring activity. The structure in the vicinity of the free syncarpic acid conjugated with a pinene moiety appears critical to the anti-scarring potential of tomentosenol A.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183299","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":"CYP2U1: a cardiac metabolic switch alleviating obesity cardiomyopathy via lipid metabolic reprogramming.","authors":"Jing Chen, Zhong-Xi Chen, Yu-Bin Lan, Rong Fang, Jing-Jing Xie, Jiang-Shun Yang, Xiao-Dan Zhang, Sui-Lin Jia, Guo-Yong Huang","doi":"10.1007/s11010-026-05773-x","DOIUrl":"https://doi.org/10.1007/s11010-026-05773-x","url":null,"abstract":"<p><p>Cytochrome P450 2U1 (CYP2U1) modulates lipid metabolism, yet its role in obesity-induced cardiomyopathy remains unknown. Here, we demonstrate that cardiac-specific overexpression of CYP2U1 safeguards against high-fat diet (HFD)-induced myocardial dysfunction. Mice received tail-vein injection of adeno-associated virus serotype 9 (AAV9) carrying CYP2U1 under the cardiac troponin T promoter (AAV9-cTnT-CYP2U1) and were maintained on a 16-week HFD. Cardiac-specific CYP2U1 overexpression was associated with better preservation of systolic function and with reduced myocardial hypertrophy, interstitial fibrosis, and cardiac inflammation. By combining transcriptomics, untargeted metabolomics, and oxylipidomics, we identified two protective mechanisms. Transcriptomic analysis indicated that CYP2U1 attenuated multiple inflammatory cascades, including nuclear factor-κB (NF-κB) p65 phosphorylation and nuclear translocation, with a corresponding reduction in interleukin-6 (IL-6) transcription; CCAAT/enhancer-binding protein β (C/EBPβ) may contribute to this regulation. Metabolomic analysis suggested that CYP2U1 remodels polyunsaturated fatty acid metabolism, consistent with a \"metabolic switch\" that shifts the balance away from pro-inflammatory arachidonic acid-derived hydroxyeicosatetraenoic acids (HETEs) toward the docosahexaenoic acid (DHA) pathway, with increased levels of the protective lipid mediators 19,20-epoxydocosapentaenoic acid (19,20-EDP) and protectin DX (PDX). In vitro, CYP2U1 overexpression in palmitic acid-challenged H9C2 cells reproduced these anti-inflammatory and metabolic features. CYP2U1 therefore limits obesity-driven cardiac inflammation by coupling suppression of the NF-κB/C/EBPβ-IL-6 axis with a shift in lipid mediators toward DHA-derived specialized pro-resolving mediators. Whether targeted activation of CYP2U1 can be translated into a therapeutic strategy for obesity-associated cardiomyopathy warrants further investigation.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183122","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":"Arbutin as a promising cardioprotective anticancer adjuvant with doxorubicin in solid Ehrlich carcinoma through targeting NEK7-dependent inflammasome/SIRT1/caspase-3/oxidative stress pathways.","authors":"Eman R Abdelmonaem, Salma M Eraky, Laila A Eissa","doi":"10.1007/s11010-026-05725-5","DOIUrl":"https://doi.org/10.1007/s11010-026-05725-5","url":null,"abstract":"<p><p>Doxorubicin (DOX) is an effective cancer therapy; however, it causes a lethal dose and time-dependent cardiotoxicity. Many patients also have cardiovascular events due to cancer itself. Therefore, our objective was to examine the antitumor effect of the natural compound arbutin and its potential cardioprotective effects against cancer and DOX-induced cardiotoxicity. Solid Ehrlich carcinoma (SEC) was established in female Swiss albino mice. DOX was administered at a dose of 6 mg/kg, ip once weekly for 21 days. A dose of 50 mg/kg ip of arbutin was administered daily for 21 consecutive days. Both tumor and heart tissues were investigated. Our results indicated that arbutin effectively reduced tumor weight and volume, both when used alone or combined with DOX, by decreasing tumor malonaldehyde and increasing glutathione levels. They also lowered tumor Sirtuin 1 (SIRT1) and increased caspase-3 expression. Unlike DOX, arbutin suppressed tumor NLR-family pyrin domain containing 3 (NLRP3), NIMA-related kinase 7 (NEK7), caspase 1, and interleukin-1-beta (IL-1β) expressions. Moreover, arbutin reduced high cardiac marker levels and attenuated cardiotoxicity by decreasing the cardiac NLRP3, NEK7, caspases 1 and 3, and IL-1β, and increasing SIRT1 expressions. Therefore, arbutin may represent a promising antitumor drug or an adjuvant therapy in the SEC model to mitigate possible cardiac issues.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137494","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":"PRDX4 ameliorates oxidative stress-induced injury in endometriosis: potential association with PTP1B oxidation and downstream phosphorylation cascades.","authors":"Yong Luo, Shanshan Zhou, Yi Zou, Ziyu Zhang, Faying Liu, Wei Jiang, Zengming Li, Liping Li","doi":"10.1007/s11010-026-05730-8","DOIUrl":"https://doi.org/10.1007/s11010-026-05730-8","url":null,"abstract":"<p><p>Oxidative stress (OS) has been proposed to play a role in the development of endometriosis (EMs). Peroxiredoxins are a family of antioxidant proteins that exhibit peroxidase activity in a thioredoxin-dependent manner, protecting cells against OS. Our previous study has shown that ROS generation is obviously increased in ectopic endometrial stromal cells with inhibition of PRXD4 expression. In our present study, IHC results indicate that the PRDX4 expression was increased in the ectopic endometria of ovarian EMs. Moreover, overexpression of PRDX4 effectively promotes cell migration. In addition, compared with vector group, overexpression of PRDX4 significantly reduces oxidative stress damage induced by H₂O₂, including increased cell viability, decreased intracellular H₂O₂ content, and reduced apoptosis rate. Interestingly, we found that the antioxidation effect of PRDX4 disappeared when the active cysteine residues (Cys124 and Cys245) were replaced with serine. To gain further insight into the antioxidant mechanism of PRDX4, our results shown that overexpression of PRDX4 decreased PTP1B oxidation and phosphorylation cascades. The in vivo findings showed that PRDX4 promoted the growth of ectopic lesions. Taken together, our results indicate that PRDX4 functions as a suppressor in injuries caused by oxidative stress, suggesting that inhibiting PRDX4 expression could be an effective treatment strategy for EMs.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137487","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":"Retraction Note: Epidermal growth factor receptor-mediated regulation of matrix metalloproteinase-2 and matrix metalloproteinase-9 in MCF-7 breast cancer cells.","authors":"Aheli Majumder, Sajal Ray, Aniruddha Banerji","doi":"10.1007/s11010-026-05763-z","DOIUrl":"https://doi.org/10.1007/s11010-026-05763-z","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112154","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":"Galloyl-RGD induces oxidative stress-mediated apoptosis in human melanoma cells.","authors":"Seo Yeon Shin, Nu Ri Song, Jae Hee Byun, Seon Ju Kim, Sun-Young Hwang, Mee-Hyun Lee, Kyung Mok Park","doi":"10.1007/s11010-026-05746-0","DOIUrl":"https://doi.org/10.1007/s11010-026-05746-0","url":null,"abstract":"<p><p>Melanoma is a malignant tumor arising from melanocytes and is characterized by rapid metastasis, making it the most aggressive form of skin cancer. Galloyl-RGD is a novel compound that combines gallic acid with RGD (Arg-Gly-Asp) tripeptide motif to overcome the problems associated with gallic acid, such as instability at high temperatures and low solubility. Although Galloyl-RGD has been previously investigated for its biological stability, regulation of melanin production, and anti-photoaging effects, its potential anticancer activity has not been clearly elucidated. In this study, proteomic profiling using two-dimensional electrophoresis and peptide mass fingerprinting suggested that Galloyl-RGD may influence melanoma cell survival and potentially trigger apoptosis-related pathways in SK-MEL28 cells. To validate these findings, we performed functional assays to evaluate the effects of Galloyl-RGD on cell viability, cell cycle progression, migration, and apoptosis in SK-MEL28 cells. Galloyl-RGD significantly reduced cell viability in SK-MEL28 melanoma cells in a dose- and time-dependent manner. It induced both early and late apoptosis and increased G1 phase arrest while reducing progression to the S and G2/M phases. Galloyl-RGD treatment elevated intracellular reactive oxygen species (ROS) levels, accompanied by activation of the stress-responsive JNK and p38 MAPK signaling pathways. In addition, the expression of key regulators associated with cell cycle progression and cell survival, including Cyclin D1, AKT/NF-κB, and Bcl-2, was markedly suppressed. Collectively, these findings demonstrate that Galloyl-RGD induces oxidative stress and modulates key survival and apoptotic signaling pathways in melanoma cells, suggesting its potential as a candidate compound targeting stress-associated mechanisms in melanoma.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112143","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":"Sphingomyelin synthase 2 deficiency suppresses airway mucus accumulation by altering sphingolipid flux and mucin glycosylation.","authors":"Harumi Sakae, Kento Sonoda, Hikari Nishisaka, Yuri Ogiso, Ryoma Miyazaki, Masaya Matsuda, Takeshi Nabe, Ken Watanabe, Toshiro Okazaki, Tomoyuki Furubayashi, Makoto Taniguchi, Kazuyuki Kitatani","doi":"10.1007/s11010-026-05753-1","DOIUrl":"https://doi.org/10.1007/s11010-026-05753-1","url":null,"abstract":"<p><p>Sphingomyelin synthase 2 (SMS2) produces sphingomyelin from ceramide. In this study, SMS2 deficiency reduced airway accumulation of glycosylated mucins, such as MUC5AC, in a murine model of asthma, prompting investigation of the molecular mechanisms in mucin-forming epithelial cells. In the cell model, SMS2 silencing promoted the conversion of ceramide to glucosylceramide, a precursor of complex glycosphingolipids. This alteration reduced MUC5AC glycosylation, suggesting the potential for biochemical competition between sphingolipids and MUC5AC for glycosylation. Supplying C₆-ceramide, which increases biochemical glycosylation for sphingolipids, reduced glycosylated MUC5AC, but this effect was absent in glucosylceramide synthase-silenced cells. These findings indicate that SMS2 deficiency alters sphingolipid metabolism, reducing MUC5AC glycosylation and maturation, underscoring the role of sphingolipid dynamics in modulating mucus production.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112288","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}