Acta biochimica et biophysica Sinica最新文献_第5页

Multicellular human cardiac organoids with real-time calcium imaging enable functional modeling of heart failure and myocardial infarction. 多细胞人类心脏类器官与实时钙成像使心力衰竭和心肌梗死的功能建模。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-10 DOI: 10.3724/abbs.2026152

Vishnu Goutham Kota, Shachin Velur Ganesan, Yin Love Ho, Samriddhi Senthilkumar, Ghazal Esfahani Maragheh, Hwa Liang Leo, Hanry Yu

{"title":"Multicellular human cardiac organoids with real-time calcium imaging enable functional modeling of heart failure and myocardial infarction.","authors":"Vishnu Goutham Kota, Shachin Velur Ganesan, Yin Love Ho, Samriddhi Senthilkumar, Ghazal Esfahani Maragheh, Hwa Liang Leo, Hanry Yu","doi":"10.3724/abbs.2026152","DOIUrl":"https://doi.org/10.3724/abbs.2026152","url":null,"abstract":"Cardiovascular diseases remain leading causes of mortality, yet progress in therapy development is limited by inadequate human-relevant models. Here, we develop a simplified, multicellular human iPSC-derived cardiac organoid system that enables functional and translational disease modeling. Using a streamlined two-component differentiation strategy, we generate robust beating cardiomyocytes and assemble three- and four-cell-type organoids incorporating endothelial cells, fibroblasts, and macrophages. Integration of a genetically encoded calcium reporter allows real-time, non-invasive functional assessment. Multicellular organoids exhibit enhanced maturation and viability, with macrophages contributing to improved functional properties. Optimized oxygen-permeable culture further enhances organoid performance. This platform recapitulates key features of overnutrition, heart failure, and myocardial infarction, including altered contractility, calcium dynamics, and biomarker expression. Together, this cost-effective and scalable system provides a physiologically relevant platform for studying cardiac disease mechanisms, drug responses, and cardiotoxicity.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928688","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}

引用次数: 0

Corrigendum to: Serum starvation induces density-dependent apoptosis via HIF-1 activation and JNK suppressio. 更正：血清饥饿通过HIF-1激活和JNK抑制诱导密度依赖性细胞凋亡。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-09 DOI: 10.3724/abbs.2026164

Qifan Yang, Yaofeng Hu, Jiahui Lv, Jiaqi Xue, Jiaqi Chen, Changwan Wang, Fajian Hou

引用次数: 0

Wogonin combined with cinnamaldehyde synergistically induces ferroptosis by increasing PTGS2 in breast cancer. Wogonin联合肉桂醛通过增加乳腺癌中PTGS2来协同诱导铁下垂。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-09 DOI: 10.3724/abbs.2026162

Shuyao Zhou, Chen Fang, Jiaqi Cui, Dajin Pi, Yuqi Liang, Qian Zuo, Jieting Chen, Junfeng Huang, Huan Shi, Qianjun Chen, Mingzi Ouyang, Yingchao Wu

{"title":"Wogonin combined with cinnamaldehyde synergistically induces ferroptosis by increasing PTGS2 in breast cancer.","authors":"Shuyao Zhou, Chen Fang, Jiaqi Cui, Dajin Pi, Yuqi Liang, Qian Zuo, Jieting Chen, Junfeng Huang, Huan Shi, Qianjun Chen, Mingzi Ouyang, Yingchao Wu","doi":"10.3724/abbs.2026162","DOIUrl":"https://doi.org/10.3724/abbs.2026162","url":null,"abstract":"Wogonin and cinnamaldehyde, extracted from the traditional Chinese herbs Scutellaria baicalensis Georgi and Cinnamomum cassia Presl, respectively, have extensive pharmacological effects. They are individually effective against breast cancer but require much higher doses than the current drugs. However, it is currently unclear whether these two natural medicines can work synergistically at low doses to achieve the effect of treating breast cancer. In this study, in vitro experiments investigate the synergistic effects of wogonin and cinnamaldehyde on suppressing breast cancer cell proliferation. Network pharmacology and bioinformatics approaches are utilized to determine the potential mechanisms and key targets underlying the therapeutic effects of wogonin and cinnamaldehyde in breast cancer, which are subsequently verified. Furthermore, animal experiments are conducted to confirm the in vivo anti-tumor effectiveness and safety of wogonin and cinnamaldehyde. The results show that wogonin and cinnamaldehyde demonstrate synergistic effects in suppressing breast cancer cell proliferation. Network pharmacology indicates that the anti-breast cancer mechanisms of wogonin and cinnamaldehyde are related to the response to oxygen-containing compounds. Bioinformatics analysis further identifies PTGS2 as a crucial target for the anti-breast cancer effects of these two natural compounds. Mechanistically, wogonin and cinnamaldehyde can synergistically promote the expression of PTGS2, thereby inducing ferroptosis in breast cancer cells. Then, in vivo validation experiments show that these two natural compounds exhibit excellent biosafety. In conclusion, wogonin and cinnamaldehyde may work synergistically to enhance PTGS2 expression at minimal doses and trigger ferroptosis in breast cancer cells, thus suppressing breast cancer progression.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975244","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}

引用次数: 0

Recombinant human SGK3 protein hydrogel: a novel therapeutic strategy for myocardial repair in ischemia/reperfusion injury. 重组人SGK3蛋白水凝胶：缺血/再灌注损伤心肌修复的新治疗策略

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-08 DOI: 10.3724/abbs.2026145

Tianwen Wei, Yuxiao Sun, Zhihao Lin, Tangjiang Wan, Yucheng Liang, Shitong Shen, Jieyun You, Qi Zhang, Yafei Li

{"title":"Recombinant human SGK3 protein hydrogel: a novel therapeutic strategy for myocardial repair in ischemia/reperfusion injury.","authors":"Tianwen Wei, Yuxiao Sun, Zhihao Lin, Tangjiang Wan, Yucheng Liang, Shitong Shen, Jieyun You, Qi Zhang, Yafei Li","doi":"10.3724/abbs.2026145","DOIUrl":"https://doi.org/10.3724/abbs.2026145","url":null,"abstract":"Myocardial infarction (MI) leads to substantial cardiomyocyte loss and heart failure, whereas current therapies fail to promote cardiac regeneration. Our prior work demonstrated that serum and glucocorticoid-regulated kinase 3 (SGK3) promote cardiac repair. To overcome the limitations of viral gene therapy, we develop a recombinant human SGK3 (rhSGK3) protein fused with a cell-penetrating peptide and encapsulate it in a thermosensitive PLGAPEG-PLGA hydrogel for sustained local delivery. In vitro, rhSGK3 efficiently enters neonatal mouse cardiomyocytes and significantly promotes proliferation, reduces OGD/R-induced apoptosis, stabilizes OGD/R-induced mitochondrial membrane potential, and upregulates the expressions of glycolytic enzymes including PKM2, LDHA, PFKP, and HK2, while shifting energy metabolism from oxidative phosphorylation toward glycolysis. These effects are reversed by the glycolysis inhibitor 2-DG. Mechanistically, rhSGK3 activates the HIF-1α/HK2 signaling axis, and HIF-1αknockdown abolishes its pro-proliferative and anti-apoptotic effects. In an in vivo myocardial ischemia/reperfusion (I/R) mouse model, intramyocardial injection of rhSGK3-hydrogel preserves mitochondrial ultrastructure, enhances cardiomyocyte proliferation, reduces apoptosis, attenuates fibrotic scar formation, and significantly improves cardiac function at 28 days post-I/R. Importantly, HIF-1α knockdown in vivo reverses these protective effects. Together, these findings suggest that local delivery of rhSGK3 via a thermosensitive hydrogel promotes cardiac repair after I/R injury through HIF-1α/HK2-mediated glycolytic reprogramming and mitochondrial protection. This study presents a promising protein-based, gene-integration-free therapeutic strategy for myocardial repair.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975317","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}

引用次数: 0

Metformin exhibits a synergistic effect with pyrotinib by inducing ferroptosis in HER2-positive cancers through the Keap1/Nrf2 pathway. 二甲双胍通过Keap1/Nrf2途径在her2阳性癌症中诱导铁凋亡，显示出与pyrotinib的协同作用。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-08 DOI: 10.3724/abbs.2026155

Yan Yang, Gaixian Shan, Huilin Li, Jianxin Hou, He Wu, Quanli Liu, Yimei He, Shan Zhao, Chunpo Ge, Bei Zhou, Jing Zhang, Yanxia Sun, Yun Yang

{"title":"Metformin exhibits a synergistic effect with pyrotinib by inducing ferroptosis in HER2-positive cancers through the Keap1/Nrf2 pathway.","authors":"Yan Yang, Gaixian Shan, Huilin Li, Jianxin Hou, He Wu, Quanli Liu, Yimei He, Shan Zhao, Chunpo Ge, Bei Zhou, Jing Zhang, Yanxia Sun, Yun Yang","doi":"10.3724/abbs.2026155","DOIUrl":"https://doi.org/10.3724/abbs.2026155","url":null,"abstract":"Human epidermal growth factor receptor 2 (HER2) overexpression plays a critical role in the progression of several cancers, driving the development of targeted therapies. However, drug resistance significantly limits the effectiveness of anti-HER2 treatments. Pyrotinib, an irreversible pan-ErbB tyrosine kinase inhibitor (TKI), and metformin, a first-line treatment for type II diabetes with anticancer properties, are potential candidates for combination therapy in HER2-positive cancers. Here we investigate the synergistic effects of pyrotinib and metformin on HER2-positive cancer cells. Our findings demonstrate that the combination of pyrotinib and metformin induces significant cell death in HER2-positive cell lines, including BT-474, SK-OV-3, and N87. Transcriptomic analysis reveals that HER2 is associated with the oxidative stress response and lipid metabolism. Mechanistically, the combination treatment primarily induces ferroptosis by reducing glutathione synthesis and impairing Fe2+ efflux, leading to excessive ROS accumulation. In vivo experiments using the SKOV-3 xenograft model show that the combination therapy significantly enhances antitumor efficacy compared to monotherapy, without causing noticeable toxicity. These results suggest that combining pyrotinib with metformin may provide an effective therapeutic strategy for HER2-positive cancers.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975153","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}

引用次数: 0

USP11-mediated deubiquitination regulates the protein stability of NR2F1. usp11介导的去泛素化调节NR2F1蛋白的稳定性。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-31 DOI: 10.3724/abbs.2026157

Ye Liu, Faliang Wu, Jinping Huang, Mengdi Cao, Yalan Wu, Hui Tang, Xiaolong Tang

引用次数: 0

Nuclear receptor Rev-erb-α mediates palmitic acid-induced lipid peroxidation in cardiomyocytes. 核受体rev - erbb -α介导棕榈酸诱导的心肌细胞脂质过氧化。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-31 DOI: 10.3724/abbs.2026132

Tingting Tan, Rujin Liang, Jinxiu Lyu, Jinyu Zhou, Yuwei Hu, Jiatong Yao, Qingliu Li, Qiujie Li, Chu Li, Dongxu Jia, Zhen Tian, Hua Zhu, Pengzhou Hang, Jing Zhao

{"title":"Nuclear receptor Rev-erb-α mediates palmitic acid-induced lipid peroxidation in cardiomyocytes.","authors":"Tingting Tan, Rujin Liang, Jinxiu Lyu, Jinyu Zhou, Yuwei Hu, Jiatong Yao, Qingliu Li, Qiujie Li, Chu Li, Dongxu Jia, Zhen Tian, Hua Zhu, Pengzhou Hang, Jing Zhao","doi":"10.3724/abbs.2026132","DOIUrl":"https://doi.org/10.3724/abbs.2026132","url":null,"abstract":"Abnormal cardiac lipid metabolism is a major contributor to cardiovascular disease (CVD). The nuclear receptor Rev-erb-α is recognized as a regulator of lipid metabolism; however, its role in cardiomyocyte lipotoxicity remains undefined. This study aims to investigate the functional role of Rev-erb-α in palmitic acid (PA)-induced lipid accumulation and peroxidation in cardiomyocytes. H9c2 cardiomyocytes are treated with the canonical Rev-erb agonists SR9009 and GSK4112 in combination with PA. Intracellular lipid droplet accumulation is quantified using Oil Red O, Nile red, and BODIPY 493/503 staining. Cytoplasmic and mitochondrial reactive oxygen species (ROS) levels are measured using 2',7'-DCFDA, dihydroethidium, and Mito-SOX probes, respectively, while DNA damage is assessed by quantifying the markers 53BP1 and γ-H2AX. Additionally, siRNA-mediated knockdown and adenovirus-mediated overexpression of Rev-erb-α are employed to validate its role in H9c2 and/or neonatal rat ventricular cardiomyocytes. PA treatment downregulates Rev-erb-α protein expression. Surprisingly, both SR9009 and GSK4112 exacerbate lipid droplet production and ROS production while activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) antioxidant pathway, independent of Rev-erb-α. However, direct adenovirus-mediated overexpression of Rev-erb-α significantly attenuates lipid droplet formation and mitochondrial ROS, which is reversed by the Nrf2 inhibitor brusatol. Mechanistically, Rev-erb-α functions as a transcriptional activator of Nrf2. Our results demonstrate a direct protective role for Rev-erb-α against lipotoxic stress and crucially reveal that its commonly used agonists have confounding, off-target pro-oxidant effects. These findings have critical implications for developing Rev-erb-α-targeted therapies for CVDs.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863035","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}

引用次数: 0

EZH2-dependent STAT3 stabilization drives pomalidomide resistance and is targetable by EZH2 inhibition in multiple myeloma. EZH2依赖性STAT3稳定驱动泊马度胺耐药，并可通过EZH2抑制多发性骨髓瘤。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-26 DOI: 10.3724/abbs.2026112

Xinyuan Zhang, Ruijing Hu, Kexin Hu, Qi Li, Linlin Qin, Yali Chai, Wenzhuo Zhuang, Xiaohui Zhang

{"title":"EZH2-dependent STAT3 stabilization drives pomalidomide resistance and is targetable by EZH2 inhibition in multiple myeloma.","authors":"Xinyuan Zhang, Ruijing Hu, Kexin Hu, Qi Li, Linlin Qin, Yali Chai, Wenzhuo Zhuang, Xiaohui Zhang","doi":"10.3724/abbs.2026112","DOIUrl":"https://doi.org/10.3724/abbs.2026112","url":null,"abstract":"Relapsed/refractory multiple myeloma (RRMM) is characterized by high mortality rates and limited survival, with real-world studies reporting substantial mortality and median survival of only a few years after relapse. Immunomodulatory drugs (IMiDs) are a cornerstone of first-line multiple myeloma (MM) therapy, yet resistance remains a major clinical challenge. Resistance to pomalidomide has been attributed to multiple mechanisms, including CRBN downregulation and activation of pro-survival signaling pathways such as NF-κB; however, the contribution of epigenetic regulators, particularly the STAT3EZH-STAT3 axis, remains insufficiently explored. In this study, our analysis of public datasets identifies significant upregulation of enhancer of zeste homolog 2 (EZH2) in RRMM patients together with an association between EZH2 expression and poor prognosis. Using two established pomalidomide-resistant MM models, we confirm elevated EZH2 expression in pomalidomide-resistant MM cell lines, and demonstrate targeting EZH2 via small interfering RNA or the selective inhibitor GSK343 elicits potent anti-myeloma effects in pomalidomide-resistant MM models. Notably, EZH2 knockdown increases the sensitivity of RRMM cells to pomalidomide, providing a rationale for combining EZH2 inhibition with pomalidomide therapy. Consistent with this observation, GSK343 synergizes with pomalidomide to suppress MM progression both in vitro and in vivo. To better understand the mechanisms involved, we conduct RNA sequencing and investigate potential mediators of EZH2. We find that EZH2 contributes to pomalidomide resistance through stabilizing STAT3 protein, thereby supporting myeloma cell survival under therapeutic stress. In conclusion, EZH2 inhibition can enhance the therapeutic efficacy of pomalidomide against RRMM, indicating that EZH2 offers a promising target for overcoming drug resistance in MM.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148823701","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}

引用次数: 0

Mining and engineering of UDP-dependent glycosyltransferases from Dendrobium officinale for trilobatin biosynthesis. 铁皮石斛中用于三叶虫苷生物合成的udp依赖糖基转移酶的挖掘和工程。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-25 DOI: 10.3724/abbs.2026136

Jiabin Huang, Pei Wen, Qinggang Yin

{"title":"Mining and engineering of UDP-dependent glycosyltransferases from Dendrobium officinale for trilobatin biosynthesis.","authors":"Jiabin Huang, Pei Wen, Qinggang Yin","doi":"10.3724/abbs.2026136","DOIUrl":"https://doi.org/10.3724/abbs.2026136","url":null,"abstract":"The development of homologous food and medicine products often involves a trade-off between maintaining a pure and natural profile and optimizing flavor. The relatively monotonous taste of Dendrobium officinale has substantially limited its market expansion. Within D. officinale, phloretin and its glycosides are present, yet the natural sweetener trilobatin (phloretin-4'- O-glucoside) is absent. Different glycosylation positions often confer distinct taste properties on specific metabolites. Following melatonin treatment, there is a predominant enrichment of flavonoid pathways in D. officinale, accompanied by a notable decrease in phloretin levels, suggesting a possible upregulation of its glycosides. Subsequently, we annotate 135 uridine diphosphate-dependent glycosyltransferases (UGTs) in D. officinale and identify three phloretin UGTs, among which the enzymatic product trilobatin has been scarcely detected. Through functional modifications of these UGTs using AlphaFold and molecular docking, we have achieved a functional shift in DoUGT885 from solely producing phlorizin to trilobatin via mutation of the M2 fragment. The alteration of fragment M5 enables DoUGT019, which originally possessed multisite glycosylation functionality for phloretin, to primarily produce trilobatin as its main enzymatic product. The discovery of these key amino acid residues crucial for trilobatin formation serves as candidate insertion or substitution sequence fragments for gene editing, significantly advancing the creation of sweet D. officinale germplasm.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817067","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}

引用次数: 0

A model for microbiota-mediated regulation and intervention of intestinal motility. 微生物介导的肠蠕动调节和干预模型。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-25 DOI: 10.3724/abbs.2026128

Zhengwen Wu

引用次数: 0