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

ANXA1 facilitates myeloid-derived suppressor cell infiltration in the non-small cell lung cancer immunomicroenvironment via the STING/NF-κB/CXCL5/CXCR2 signaling axis to enhance tumor progression. ANXA1通过STING/NF-κB/CXCL5/CXCR2信号轴促进非小细胞肺癌免疫微环境中髓源性抑制细胞浸润，促进肿瘤进展。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-07-03 DOI: 10.1016/j.bbadis.2025.167965

Xinyue Liu, Xiangtian Xiao, Yanqi Feng, Yiming Li, Shuxi Yao, Yuelin Han, Shu Xia

{"title":"ANXA1 facilitates myeloid-derived suppressor cell infiltration in the non-small cell lung cancer immunomicroenvironment via the STING/NF-κB/CXCL5/CXCR2 signaling axis to enhance tumor progression.","authors":"Xinyue Liu, Xiangtian Xiao, Yanqi Feng, Yiming Li, Shuxi Yao, Yuelin Han, Shu Xia","doi":"10.1016/j.bbadis.2025.167965","DOIUrl":"https://doi.org/10.1016/j.bbadis.2025.167965","url":null,"abstract":"The infiltration of immune cells within the tumor microenvironment is a crucial determinant of the therapeutic efficacy of cancer immunotherapy. In non-small cell lung cancer (NSCLC), elucidating the regulatory mechanisms that govern the immune microenvironment is of substantial clinical importance. This study identifies Annexin A1 (ANXA1) as a key mediator in promoting the establishment of an immunosuppressive microenvironment driven by tumor cells. Clinical findings demonstrate that increased ANXA1 expression in NSCLC is highly correlated with worse prognosis and reduced effectiveness of immunotherapy. Complementary in vivo experiments further demonstrate that ANXA1 facilitates subcutaneous tumor progression and enhances the recruitment of myeloid-derived suppressor cells (MDSCs), thus fostering an immunosuppressive tumor microenvironment. Mechanistically, ANXA1 modulates the methylation status of UHRF1 (Ubiquitin-like plant homeodomain and RING finger domain-containing protein 1), disrupting DNA damage repair processes and leading to the accumulation of cytosolic double-stranded DNA (dsDNA), which triggers the activation of the STING/NF-κB/CXCL5 signaling axis. CXCL5 binds to its receptor CXCR2 on MDSCs, thereby promoting their recruitment. Importantly, inhibition of CXCR2 effectively reverses ANXA1-mediated MDSCs infiltration. These results elucidate the essential function of ANXA1 in modulating the recruitment of MDSCs within the immune environment of NSCLC, establishing ANXA1 as a significant therapeutic target for the advancement of innovative immunotherapeutic approaches.","PeriodicalId":93896,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":" ","pages":"167965"},"PeriodicalIF":0.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568212","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

Advances in clinical studies of peptide drugs in stroke disease. 脑卒中多肽药物的临床研究进展。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-07-02 DOI: 10.1016/j.bbadis.2025.167970

Yan Huo, Zhe Zhang, Suzhen Dong, Yijie Du, Mingliang Ma

引用次数: 0

Special issue - Mitochondria in aging, cancer and cell death. 特刊-线粒体在衰老，癌症和细胞死亡。

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-06-17 DOI: 10.1016/j.bbadis.2025.167954

Ana M Urbano, Paulo J Oliveira

引用次数: 0

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

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