Biochimica et biophysica acta. Molecular basis of disease最新文献

High fluid shear stress induces Hippo/YAP pathway in articular cartilage superficial layer cells: A potential mechanistic link to osteoarthritis. 高流体剪切应力诱导关节软骨浅层细胞的Hippo/YAP通路：与骨关节炎的潜在机制联系

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-05-29 DOI: 10.1016/j.bbadis.2025.167939

Haitao Li, Yuxuan Ou, Lifu Chen, Yong Li, Wei Wang, Jian Wang

{"title":"High fluid shear stress induces Hippo/YAP pathway in articular cartilage superficial layer cells: A potential mechanistic link to osteoarthritis.","authors":"Haitao Li, Yuxuan Ou, Lifu Chen, Yong Li, Wei Wang, Jian Wang","doi":"10.1016/j.bbadis.2025.167939","DOIUrl":"https://doi.org/10.1016/j.bbadis.2025.167939","url":null,"abstract":"Abnormal mechanical loading, which can lead to articular cartilage damage, is a significant contributor to the onset of osteoarthritis (OA). Articular cartilage superficial layer cells are among the first cells to respond to changes in the mechanical environment and are highly sensitive to mechanical stimuli. This study aimed to investigate the effects of high fluid shear stress on the articular cartilage superficial layer cells and the underlying mechanisms. We found that high fluid shear stress of 20 dyne/cm2 induces inflammation and promotes catabolic processes in these cells. Short-term high fluid shear stress has a protective effect, but its efficacy varies with time. YAP plays a crucial role in mediating the effects of high fluid shear stress and may represent a potential therapeutic target for early-stage osteoarthritis. The study also established osteoarthritis models using anterior cruciate ligament transection (ACLT) or injection of sodium iodoacetate (MIA) to further confirm the findings.","PeriodicalId":93896,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":" ","pages":"167939"},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Combined inhibition of EGFR and FGFRs with Cetuximab and Infigratinib showed effectiveness and relevance in proliferation and migration of HNSCC cell lines. 西妥昔单抗和消炎替尼联合抑制EGFR和fgfr显示出对HNSCC细胞系增殖和迁移的有效性和相关性。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-05-29 DOI: 10.1016/j.bbadis.2025.167940

Monika Orsolic, Marc Diensthuber, Timo Stöver, Christin Geißler

{"title":"Combined inhibition of EGFR and FGFRs with Cetuximab and Infigratinib showed effectiveness and relevance in proliferation and migration of HNSCC cell lines.","authors":"Monika Orsolic, Marc Diensthuber, Timo Stöver, Christin Geißler","doi":"10.1016/j.bbadis.2025.167940","DOIUrl":"https://doi.org/10.1016/j.bbadis.2025.167940","url":null,"abstract":"Head and neck squamous cell carcinoma (HNSCC) presents significant oncological challenges, necessitating novel treatments due to high global mortality. The current study focuses on the potential of combining Cetuximab (CTX), targeting EGFR, and Infigratinib (BGJ), targeting FGFRs, to improve treatment outcomes. The effects of CTX and BGJ on HNSCC cell lines were investigated by analyzing cell count and gap closure to assess proliferation and migration. Immunohistochemistry was used to assess EGFR and FGFRs expressions, and responses to related growth factors were studied. CTX primarily reduced gap closure in migration assay, while BGJ reduced cell counts more obviously. Combined application enhanced performance in three out of four cell lines. All cell lines exhibited high EGFR expression, while KGFR expression was observed in a subpopulation. EGF stimulation led to cell elongation and an increase in size in three cell lines, accompanied by notable changes in migration. KGF impacted cell morphology and migration in one cell line. This study shows that combination of CTX and BGJ was most effective against cell lines, highlighting the crucial roles of EGFR and KGFR, with KGFR potentially mediating effects of BGJ. The findings suggest that adding targeted therapies for receptors on relevant cell subpopulations may enhance outcomes in therapy.","PeriodicalId":93896,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":" ","pages":"167940"},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "CXCL12 derived from CD248-expressing cancer-associated fibroblasts mediates M2-polarized macrophages to promote nonsmall cell lung cancer progression" [Biochim. Biophys. Acta Mol. Basis Dis., 1868 (2022) 166521-166521/10.1016/j.bbadis.2022.166521]. “从表达cd248的癌症相关成纤维细胞衍生的CXCL12介导m2极化巨噬细胞促进非小细胞肺癌进展”的更正[biochem]。Biophys。分子基础疾病学报，1868 (2022)166521-166521/10.1016/j.b adis.2022.166521。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-26 DOI: 10.1016/j.bbadis.2025.167864

Jieheng Wu, Xinlei Liu, Jiangwei Wu, Chunju Lou, Qiaoling Zhang, Huiping Chen, Zeyang Yang, Shiqi Long, Yun Wang, Zhenling Shang, Zuquan Hu, Rui Zhang, Jian Zhang, Zhu Zeng

引用次数: 0

Retraction notice to "Leptin attenuates BACE1 expression and amyloid-β genesis via the activation of SIRT1 signaling pathway" [Biochim. Biophys. Acta (BBA) - Mol. Basis Dis. 1842 (2014) 1587-1595]. “Leptin通过激活SIRT1信号通路减弱BACE1表达和淀粉样蛋白-β的形成”的撤回通知[biochem]。Biophys。[j].生物化学学报，2014,42(2014):1587-1595。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-25 DOI: 10.1016/j.bbadis.2025.167860

Gurdeep Marwarha, Shaneabbas Raza, Craig Meiers, Othman Ghribi

引用次数: 0

An epigenetic perspective of viral diseases, including cancer and autophagy. 病毒疾病的表观遗传学观点，包括癌症和自噬。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-03-01 Epub Date: 2025-01-10 DOI: 10.1016/j.bbadis.2025.167664

Samir Kumar Patra

引用次数: 0

A potential early-atheroprotective target: Irgm1 mediates lymphangiogenesis through LEC autophagy by Tfeb translocation. 潜在的早期动脉粥样硬化保护靶标：Irgm1 通过 Tfeb 转位介导淋巴管自噬。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2024-08-01 Epub Date: 2024-05-15 DOI: 10.1016/j.bbadis.2024.167238

Hengxuan Cai, Guanpeng Ma, Zhenming Zhang, Guojie Liu, Rongzhe Lu, Yige Liu, Jiaxin Wang, Shanjie Wang, Song Sun, Mingyan E, Zhaoying Li, Shaohong Fang, Bo Yu

{"title":"A potential early-atheroprotective target: Irgm1 mediates lymphangiogenesis through LEC autophagy by Tfeb translocation.","authors":"Hengxuan Cai, Guanpeng Ma, Zhenming Zhang, Guojie Liu, Rongzhe Lu, Yige Liu, Jiaxin Wang, Shanjie Wang, Song Sun, Mingyan E, Zhaoying Li, Shaohong Fang, Bo Yu","doi":"10.1016/j.bbadis.2024.167238","DOIUrl":"10.1016/j.bbadis.2024.167238","url":null,"abstract":"Lymphatic dysfunction is a pivotal pathological mechanism underlying the development of early atherosclerotic plaques. Potential targets of lymphatic function must be identified to realize the early prevention and treatment of atherosclerosis (AS). The immunity-related GTPase Irgm1 is involved in orchestrating cellular autophagy and apoptosis. However, the effect of Irgm1 on early AS progression, particularly through alterations in lymphatic function, remains unclear. In this study, we confirmed the protective effect of lymphangiogenesis on early-AS in vivo. Subsequently, an in vivo model of early AS mice with Irgm1 knockdown shows that Irgm1 reduces early atherosclerotic plaque burden by promoting lymphangiogenesis. Given that lymphatic endothelial cell (LEC) autophagy significantly contributes to lymphangiogenesis, Irgm1 may enhance lymphatic circulation by promoting LEC autophagy. Moreover, Irgm1 orchestrates autophagy in LECs by inhibiting mTOR and facilitating nuclear translocation of Tfeb. Collectively, these processes lead to lymphangiogenesis. Thus, this study establishes a link between Irgm1 and early AS, thus revealing a novel mechanism by which Irgm1 exerts an early protective influence on AS within the context of lymphatic circulation. The insights gained from this study have the potential to revolutionize the approach and management of AS onset.","PeriodicalId":93896,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":" ","pages":"167238"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140960797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "Exogenous recombinant N-acetylgalactosamine-4-sulfatase (Arylsulfatase B; ARSB) inhibits progression of B16F10 cutaneous melanomas and modulates cell signaling" [Biochim. Biophys. Acta Mol. Basis Dis. 1870(1) (2024)166913-25, PMID: 37813168]. 外源重组 N-乙酰半乳糖胺-4-硫酸酯酶（Arylsulfatase B; ARSB）抑制 B16F10 皮肤黑色素瘤的进展并调节细胞信号传导》[Biochim.Biochim.Acta Mol.Basis Dis.1870(1) (2024)166913-25, PMID: 37813168]。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2024-05-16 DOI: 10.1016/j.bbadis.2024.167231

Sumit Bhattacharyya, Insug O-Sullivan, Jieqi Tu, Zhengjia Chen, Joanne K Tobacman

引用次数: 0