IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-21 eCollection Date: 2025-01-01 DOI: 10.34133/research.0951

Jingjia Ye, Fenglu Li, Zhengfa Wen, Junsheng He, Gaoxing Pan, Xinrang Zhai, Linran Song, Xianzhu Zhang, Xuefei Zhou, Xudong Yao, Yanlang Wang, Jin Zhang, Wei Wei

{"title":"Multichannel 3D-Printed Bioactive Scaffold Combined with Small Interfering RNA Delivery to Promote Neurological Recovery after Spinal Cord Injury.","authors":"Jingjia Ye, Fenglu Li, Zhengfa Wen, Junsheng He, Gaoxing Pan, Xinrang Zhai, Linran Song, Xianzhu Zhang, Xuefei Zhou, Xudong Yao, Yanlang Wang, Jin Zhang, Wei Wei","doi":"10.34133/research.0951","DOIUrl":"https://doi.org/10.34133/research.0951","url":null,"abstract":"Enhancing axonal regeneration holds promise for restoring neural circuits and locomotion function after spinal cord injury (SCI), while precise guidance of micrometer-scale axons to their natural regions remains a critical challenge. To address this problem, we developed an integrated 3D-printed scaffold featuring internal parallel channels infused with a bioactive hydrogel containing laminin-derived chimeric RADA4-IKVAV peptide. This scaffold combined physical guidance cues with molecular modulation synergistically by constructing an incorporated small interfering RNA delivery platform targeting phosphatase and tensin homolog. Comprehensive validations via immunohistochemistry, single-cell RNA sequencing, and behavioral assays demonstrated that this approach effectively protected surrounding tissues in lesion area, enhanced ability of axonal regeneration, and improved locomotion functional recovery of rats significantly. Mechanistic investigations further revealed that the introduced IKVAV peptide specifically up-regulated Ephrin/Eph signaling pathway genes, driving establishment of functional axon networks. Overall, this strategy potentially helps to develop new clinical approach for efficiently treating SCI.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0951"},"PeriodicalIF":10.7,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Locust-Derived Biohybrid Muscle Actuators for Low-Power Explosive Jumping. 用于低功率爆炸跳跃的蝗虫衍生生物杂交肌肉驱动器。

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-21 eCollection Date: 2025-01-01 DOI: 10.34133/research.0943

Peng Liu, Yao Li, Songsong Ma, Yunhao Si, Bing Li

{"title":"Locust-Derived Biohybrid Muscle Actuators for Low-Power Explosive Jumping.","authors":"Peng Liu, Yao Li, Songsong Ma, Yunhao Si, Bing Li","doi":"10.34133/research.0943","DOIUrl":"https://doi.org/10.34133/research.0943","url":null,"abstract":"A critical challenge for jumping microrobots is achieving a compact actuator with a high energy output as traditional elastic actuators are inherently bulky. The integration of biological materials with artificial systems to realize biohybrid muscle actuators is a promising approach. However, previous attempts utilizing the entire organism have been hampered by the unpredictability of the native nervous system, and actuators integrating cultivated or extracted muscle tissues have so far been unable to achieve a sufficiently explosive output capacity for jumping. Here, discarded locust hindlegs are repurposed into explosive biohybrid muscle actuators that are synergistically integrated with an artificial robotic system. The resulting biohybrid locust is only 2 g in weight and is precisely controlled through electrical stimulation to achieve dynamic leaps of up to 18 times its body length and 7 times its body height, which outperforms most synthetic counterparts. The design exhibits 2 key functional advances: on the one hand, the actuator requires an ultralow-power input of only 0.03 mW via the optimization of stimulation protocols; on the other hand, the actuator rapidly releases kinetic energy, enabling the artificial robotic system to perform long-distance jumps. This paper presents an experimental validation and biomechanical analysis on the biohybrid locust to demonstrate how our strategy unlocks sustainable and high-performance actuation for microrobots. This work pioneers a roadmap for the next generation of biohybrid robots that merge ecological sustainability with engineering excellence.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0943"},"PeriodicalIF":10.7,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chronic Psychological Stress in Oncogenesis: Multisystem Crosstalk and Multimodal Interventions. 肿瘤发生中的慢性心理应激：多系统串扰和多模式干预。

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-21 eCollection Date: 2025-01-01 DOI: 10.34133/research.0948

Bin Huang, Honglin An, Han Wu, Yiman Qiu, Yanqing Su, Liming Chen, Vasiliki Epameinondas Georgakopoulou, Jiumao Lin, Wujin Chen, Ruofei Li, Dongliang Yang, Xiaojiaoyang Li, Demetrios A Spandidos

{"title":"Chronic Psychological Stress in Oncogenesis: Multisystem Crosstalk and Multimodal Interventions.","authors":"Bin Huang, Honglin An, Han Wu, Yiman Qiu, Yanqing Su, Liming Chen, Vasiliki Epameinondas Georgakopoulou, Jiumao Lin, Wujin Chen, Ruofei Li, Dongliang Yang, Xiaojiaoyang Li, Demetrios A Spandidos","doi":"10.34133/research.0948","DOIUrl":"https://doi.org/10.34133/research.0948","url":null,"abstract":"Malignant tumors constitute a major global public health burden. Chronic psychological stress (CPS) manifests as sustained dysregulation arising from prolonged adaptive responses to chronic endogenous and exogenous stimuli. Clinical evidence indicates that CPS markedly influences cancer progression, with most oncology patients developing detectable stress-related psychological disorders during disease management. This review synthesizes recent advances in understanding CPS-mediated oncogenic mechanisms and evaluates current intervention approaches. Mechanistically, CPS compromises immune surveillance through neuroendocrine-mediated hormonal dysregulation, impairing malignant cell recognition and clearance. Concurrently, CPS hormones promote tumor metabolic adaptation via hypothalamic-pituitary-adrenal axis-driven metabolic reprogramming, enhancing glycolytic flux to support uncontrolled proliferation. CPS further accelerates tumor progression through reactive oxygen species-induced mitochondrial impairment, DNA damage accumulation, and inflammatory cascades. Notably, CPS induces gut microbiota perturbations that reciprocally amplify tumorigenic processes through microbial metabolite disturbances and neuroimmune crosstalk, creating a self-perpetuating pathogenic loop. Therapeutic strategies to address cancer-related CPS that encompass pharmacological agents targeting neuroendocrine pathways, psychosomatic behavioral interventions, social environment adjustments, and evidence-based traditional Chinese medicine formulations demonstrate potential in cancer prevention, treatment, and outcome optimization. However, challenges remain in achieving precise neuromodulation and minimizing intervention side effects, underscoring the need for mechanism-guided therapeutic innovations.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0948"},"PeriodicalIF":10.7,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ultralow Lattice Thermal Conductivity and High ZT of n-Type Polycrystalline SnSe Realized by Liquid Phase Sintering. 液相烧结实现n型多晶SnSe的超低点阵热导率和高ZT。

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-21 eCollection Date: 2025-01-01 DOI: 10.34133/research.0962

Bin Su, Yilin Jiang, Hua-Lu Zhuang, Zhanran Han, Jincheng Yu, Haihua Hu, Jing-Wei Li, Hezhang Li, Yu-Xiao He, Lu Chen, Zhengqin Wang, Jing-Feng Li

{"title":"Ultralow Lattice Thermal Conductivity and High ZT of n-Type Polycrystalline SnSe Realized by Liquid Phase Sintering.","authors":"Bin Su, Yilin Jiang, Hua-Lu Zhuang, Zhanran Han, Jincheng Yu, Haihua Hu, Jing-Wei Li, Hezhang Li, Yu-Xiao He, Lu Chen, Zhengqin Wang, Jing-Feng Li","doi":"10.34133/research.0962","DOIUrl":"https://doi.org/10.34133/research.0962","url":null,"abstract":"SnSe has drawn increasing attention in thermoelectric applications because of its exceptional n/p-type characteristics. Although recent studies have reported an excellent figure of merit (ZT) value in p-type polycrystalline SnSe, achieving a breakthrough in thermoelectric performance for its n-type counterpart SnSe remains a critical challenge. The presence of VSn imposes a critical constraint on the synergistic optimization of carrier transport and phonon scattering in n-type SnSe. In this study, liquid phase sintering introduces high-density dislocations into n-type SnSe polycrystals, effectively scattering mid-frequency phonons. Huge lattice strain fluctuations caused by the defects enable an ultralow lattice thermal conductivity (0.21 W m-1 K-1) at 793 K. In addition, part of the liquid phase Sn tends to penetrate into the matrix, which leads to a higher carrier concentration and considerable enhancement in electrical properties. Consequently, a superior ZT (~1.9, 793 K) and an outstanding average ZT (ZT ave) (~0.72, 300 to 873 K) are achieved in polycrystalline SnSe, which rank at the top level reported for SnSe-based n-type thermoelectric materials, exceeding those of most n-type thermoelectric systems for mid-temperature applications.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0962"},"PeriodicalIF":10.7,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Paclitaxel Biosynthesis Pathway Unlocked. 紫杉醇生物合成途径解锁

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-21 eCollection Date: 2025-01-01 DOI: 10.34133/research.0965

Laure Martinelli, Nicolas Papon, Vincent Courdavault

引用次数: 0

Na⁺/K⁺-ATPase Modulates Purinergic P2X3 Receptor Function to Drive Bone Cancer Pain. Na+/K+- atp酶调节嘌呤能P2X3受体功能驱动骨癌疼痛

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-20 eCollection Date: 2025-01-01 DOI: 10.34133/research.0932

Songqiang Huang, Bo Peng, Wanting Dong, Jiapeng He, Hanbin Chen, Jin-Song Bian

{"title":"Na+/K+-ATPase Modulates Purinergic P2X3 Receptor Function to Drive Bone Cancer Pain.","authors":"Songqiang Huang, Bo Peng, Wanting Dong, Jiapeng He, Hanbin Chen, Jin-Song Bian","doi":"10.34133/research.0932","DOIUrl":"https://doi.org/10.34133/research.0932","url":null,"abstract":"Bone cancer pain (BCP) is one of the most common types of chronic pain in cancer patients, with a prevalence of up to 75%. However, the pathological mechanism and therapeutic approaches are limited. Here, we demonstrated that Na+/K+-ATPase α1 (NKAα1) is a critical regulator of nociception through interaction with purinergic P2X3 receptor (P2X3R) in the dorsal root ganglion (DRG). Conditional knockout of NKAα1 in transient receptor potential vanilloid 1-positive (TRPV1+) neurons led to an increase in P2X3R-dependent Ca2+ influx and neuronal hyperexcitability and also promoted pain hypersensitivity in BCP model mice. In addition, NKAα1 knockout in TRPV1+ neurons further enhanced C-C motif chemokine ligand 5 release, thereby exacerbating spinal glial cell activation and pain hypersensitivity in BCP mice. DR5-12D, a monoclonal antibody to stabilize the expression of NKAα1, markedly inhibited the hyperexcitability of DRG nociceptors and ameliorated pain hypersensitivity in BCP mice. Overall, NKAα1 modulates P2X3R-dependent Ca2+ influx and the excitability of DRG nociceptors, thereby providing valuable theoretical guidance for the treatment of BCP.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0932"},"PeriodicalIF":10.7,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12536475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tubular-Cell-Derived Extracellular Vesicle miR-491-3p Aggravates Renal Ischemia-Reperfusion Injury by Inhibiting Macrophage SIRT1-Mediated Notch Intracellular Domain Deacetylation-Driven Ubiquitin-Proteasome Degradation. 小管细胞来源的细胞外泡miR-491-3p通过抑制巨噬细胞sirt1介导的Notch胞内结构域去乙酰化驱动的泛素蛋白酶体降解加重肾缺血再灌注损伤

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-17 eCollection Date: 2025-01-01 DOI: 10.34133/research.0929

Peihan Wang, Bojun Li, Tianbao Song, Zefeng Wang, Zhen Yin, Baofeng Song, Sheng Zhao, Xiangjun Zhou, Weimin Yu, Fan Cheng, Wei Li

{"title":"Tubular-Cell-Derived Extracellular Vesicle miR-491-3p Aggravates Renal Ischemia-Reperfusion Injury by Inhibiting Macrophage SIRT1-Mediated Notch Intracellular Domain Deacetylation-Driven Ubiquitin-Proteasome Degradation.","authors":"Peihan Wang, Bojun Li, Tianbao Song, Zefeng Wang, Zhen Yin, Baofeng Song, Sheng Zhao, Xiangjun Zhou, Weimin Yu, Fan Cheng, Wei Li","doi":"10.34133/research.0929","DOIUrl":"10.34133/research.0929","url":null,"abstract":"Renal ischemia-reperfusion injury triggers substantial inflammatory reactions, with renal tubular epithelial cells (TECs) and macrophages playing crucial roles. Extracellular vesicles (EVs) are key mediators of intercellular signaling. However, the precise roles and mechanisms by which TEC-derived EVs influence macrophage functions remain unclear. This study investigated how miR-491-3p within EVs from TECs modulates macrophage polarization, thus worsening renal inflammation and damage. In models that are in vitro and in vivo, EVs enriched with miR-491-3p from TECs subjected to hypoxia/reoxygenation were shown to promote M1 polarization in macrophages, enhancing inflammatory responses and inducing TEC apoptosis. Mechanistically, miR-491-3p directly targets sirtuin 1 (SIRT1) in macrophages, inhibiting SIRT1-mediated Notch intracellular domain (NICD) deacetylation, thereby regulating NICD stability. This regulation blocks F-box and WD repeat domain-containing 7 (FBXW7)-NICD binding, reduces NICD ubiquitination, and activates the Notch/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Furthermore, Rab27a knockout, which limits EVs' release, substantially reduces M1 macrophage polarization and renal tissue damage. These findings indicate that miR-491-3p from TEC-derived EVs targets SIRT1, inhibiting the deacetylation of NICD mediated by SIRT1, which subsequently prevents ubiquitin-mediated NICD degradation. This mechanism modulates the inflammatory phenotype of macrophages and promotes the inflammatory response, thereby worsening renal injury induced by ischemia-reperfusion injury and highlighting a potential therapeutic target.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0929"},"PeriodicalIF":10.7,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12531491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exploring Biomass Precursor Synthesis as a Determinant in Microbial Adaptation to Unadapted Carbon Sources with AdaptUC. 利用AdaptUC探索生物质前体合成作为微生物适应不适应碳源的决定因素。

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-17 eCollection Date: 2025-01-01 DOI: 10.34133/research.0881

Jingyi Cai, Jiayu Liu, Fan Wei, Wenjun Wu, Wenqi Xu, Yu Wang, Qianqian Yuan, Hongwu Ma

{"title":"Exploring Biomass Precursor Synthesis as a Determinant in Microbial Adaptation to Unadapted Carbon Sources with AdaptUC.","authors":"Jingyi Cai, Jiayu Liu, Fan Wei, Wenjun Wu, Wenqi Xu, Yu Wang, Qianqian Yuan, Hongwu Ma","doi":"10.34133/research.0881","DOIUrl":"10.34133/research.0881","url":null,"abstract":"Industrial microorganisms often struggle to utilize renewable substrates such as methanol, formate, and xylose. Here, we introduce AdaptUC, a computational framework that demonstrates how the fraction of biomass precursors synthesized from unadapted carbon sources governs both the evolutionary driving force and the minimal substrate requirement. AdaptUC predicts gene knockout strategies for constructing the starting strain for adaptive laboratory evolution by selectively blocking metabolic pathways, thereby rendering specific precursor pools dependent on the unadapted substrate. We show that smaller dependency fractions correspond to higher driving forces for evolution of the starting strain. Case studies in Escherichia coli and Corynebacterium glutamicum, validated against experimental records and literature, confirm AdaptUC's ability to identify knockout combinations that fine-tune precursor dependency and accelerate adaptation. By leveraging genome-scale metabolic models, AdaptUC navigates vast candidate pools without combinatorial explosion, reducing experimental screening and prioritizing strains with stronger evolutionary drives.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0881"},"PeriodicalIF":10.7,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12531492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cardiovascular Information and Health Engineering Medicine. 心血管信息与健康工程医学“，”

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-17 eCollection Date: 2025-01-01 DOI: 10.34133/research.0956

Xue Bao, Ziyu Zhang, Yuhe Shen, Peng Tang, Guangxiang Si, Lina Kang, Biao Xu, Ning Gu

{"title":"Cardiovascular Information and Health Engineering Medicine.","authors":"Xue Bao, Ziyu Zhang, Yuhe Shen, Peng Tang, Guangxiang Si, Lina Kang, Biao Xu, Ning Gu","doi":"10.34133/research.0956","DOIUrl":"10.34133/research.0956","url":null,"abstract":"Cardiovascular diseases (CVDs) persistently impose a substantial global health burden, highlighting the necessity for innovative approaches to their prevention, diagnosis, and treatment. This paper accentuates the close correlation between vascular health and CVDs. To address unmet clinical demands for the early and efficient management of CVDs, we emphasize the potential of engineering medicine and propose the concept of cardiovascular information and health engineering medicine (CVIHEM), delineating its objectives and framework for collecting, analyzing, and translating multidimensional vascular data into practical strategies. By systematically and efficiently acquiring and translating vascular information through multidisciplinary collaboration, CVIHEM enhances our understanding of the vascular network and provides innovative strategies for promoting vascular health. This approach encompasses a range of applications, such as artificial intelligence-driven decision-making, targeted therapy, and vascular health management, ultimately improving vascular health and clinical outcomes.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0956"},"PeriodicalIF":10.7,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12531494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HDAC11-Mediated Deacetylation of Triosephosphate Isomerase 1 Promotes Idiopathic Pulmonary Fibrosis. hdac11介导的三磷酸异构酶1去乙酰化促进特发性肺纤维化。

IF 10.7 1区综合性期刊

Research Pub Date : 2025-10-16 eCollection Date: 2025-01-01 DOI: 10.34133/research.0953

Yu Li, Xiangguang Shi, Feiyang Zhang, Xiumin Zhou, Xinyu Zhu, Jiawei Chen, Kai Fu, Jun Chen, Jian Yang, Zhike Chen, Xin Tong, Jun Zhao, Chang Li

{"title":"HDAC11-Mediated Deacetylation of Triosephosphate Isomerase 1 Promotes Idiopathic Pulmonary Fibrosis.","authors":"Yu Li, Xiangguang Shi, Feiyang Zhang, Xiumin Zhou, Xinyu Zhu, Jiawei Chen, Kai Fu, Jun Chen, Jian Yang, Zhike Chen, Xin Tong, Jun Zhao, Chang Li","doi":"10.34133/research.0953","DOIUrl":"10.34133/research.0953","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is a type of chronic progressive fibrotic interstitial pneumonia and has a poor prognosis due to the lack of effective treatments. Despite extensive investigations into its molecular and cellular mechanisms, the regulatory mechanism involved remains incompletely understood. Triosephosphate isomerase 1 (TPI1), an enzyme in the glycolytic pathway, has emerged as a key research focus in oncogenesis due to its multifaceted roles in malignant progression. However, its role in IPF has not yet been reported. Here, we report that TPI1 expression was elevated in IPF tissues and in mice with bleomycin-induced pulmonary fibrosis. TPI1 knockdown attenuated IPF progression in vitro and in vivo. Mechanistically, we found that histone deacetylase 11 (HDAC11)-mediated deacetylation of TPI1 K69 was enhanced by transforming growth factor-beta1. Deacetylation of TPI1 K69 enhanced its protein stability by attenuating K48-linked polyubiquitination, which enhanced fibroblast-to-myofibroblast differentiation, cell proliferation, and migration. Notably, we designed and tested the activity of a novel cell-penetrating peptide that increased the acetylation of TPI1 and markedly promoted TPI1 degradation, thereby effectively reducing fibrosis. Together, our findings revealed that targeting TPI1 acetylation is an effective strategy for IPF therapy, and the specific cell-penetrating peptide could prevent IPF by promoting the acetylation of TPI1.","PeriodicalId":21120,"journal":{"name":"Research","volume":"8 ","pages":"0953"},"PeriodicalIF":10.7,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12529298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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