Acta Pharmaceutica Sinica. B最新文献

英文中文

Extracellular vesicles deliver thioredoxin to rescue stem cells from senescence and intervertebral disc degeneration via a feed-forward circuit of the NRF2/AP-1 composite pathway

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.12.013

Xuanzuo Chen , Sheng Liu , Huiwen Wang , Yiran Liu , Yan Xiao , Kanglu Li , Feifei Ni , Wei Wu , Hui Lin , Xiangcheng Qing , Feifei Pu , Baichuan Wang , Zengwu Shao , Yizhong Peng

Intervertebral disc degeneration (IDD) is largely attributed to impaired endogenous repair. Nucleus pulposus-derived stem cells (NPSCs) senescence leads to endogenous repair failure. Small extracellular vesicles/exosomes derived from mesenchymal stem cells (mExo) have shown great therapeutic potential in IDD, while whether mExo could alleviate NPSCs senescence and its mechanisms remained unknown. We established a compression-induced NPSCs senescence model and rat IDD models to evaluate the therapeutic efficiency of mExo and investigate the mechanisms. We found that mExo significantly alleviated NPSCs senescence and promoted disc regeneration while knocking down thioredoxin (TXN) impaired the protective effects of mExo. TXN was bound to various endosomal sorting complex required for transport (ESCRT) proteins. Autocrine motility factor receptor (AMFR) mediated TXN K63 ubiquitination to promote the binding of TXN on ESCRT proteins and sorting of TXN into mExo. Knocking down exosomal TXN inhibited the transcriptional activity of nuclear factor erythroid 2-related factor 2 (NRF2) and activator protein 1 (AP-1). NRF2 and AP-1 inhibition reduced endogenous TXN production that was promoted by exosomal TXN. Inhibition of NRF2 in vivo diminished the anti-senescence and regenerative effects of mExo. Conclusively, AMFR-mediated TXN ubiquitination promoted the sorting of TXN into mExo, allowing exosomal TXN to promote endogenous TXN production in NPSCs via TXN/NRF2/AP-1 feed-forward circuit to alleviate NPSCs senescence and disc degeneration.

{"title":"Extracellular vesicles deliver thioredoxin to rescue stem cells from senescence and intervertebral disc degeneration via a feed-forward circuit of the NRF2/AP-1 composite pathway","authors":"Xuanzuo Chen , Sheng Liu , Huiwen Wang , Yiran Liu , Yan Xiao , Kanglu Li , Feifei Ni , Wei Wu , Hui Lin , Xiangcheng Qing , Feifei Pu , Baichuan Wang , Zengwu Shao , Yizhong Peng","doi":"10.1016/j.apsb.2024.12.013","DOIUrl":"10.1016/j.apsb.2024.12.013","url":null,"abstract":"<div><div>Intervertebral disc degeneration (IDD) is largely attributed to impaired endogenous repair. Nucleus pulposus-derived stem cells (NPSCs) senescence leads to endogenous repair failure. Small extracellular vesicles/exosomes derived from mesenchymal stem cells (mExo) have shown great therapeutic potential in IDD, while whether mExo could alleviate NPSCs senescence and its mechanisms remained unknown. We established a compression-induced NPSCs senescence model and rat IDD models to evaluate the therapeutic efficiency of mExo and investigate the mechanisms. We found that mExo significantly alleviated NPSCs senescence and promoted disc regeneration while knocking down thioredoxin (TXN) impaired the protective effects of mExo. TXN was bound to various endosomal sorting complex required for transport (ESCRT) proteins. Autocrine motility factor receptor (AMFR) mediated TXN K63 ubiquitination to promote the binding of TXN on ESCRT proteins and sorting of TXN into mExo. Knocking down exosomal TXN inhibited the transcriptional activity of nuclear factor erythroid 2-related factor 2 (NRF2) and activator protein 1 (AP-1). NRF2 and AP-1 inhibition reduced endogenous TXN production that was promoted by exosomal TXN. Inhibition of NRF2 <em>in vivo</em> diminished the anti-senescence and regenerative effects of mExo. Conclusively, AMFR-mediated TXN ubiquitination promoted the sorting of TXN into mExo, allowing exosomal TXN to promote endogenous TXN production in NPSCs <em>via</em> TXN/NRF2/AP-1 feed-forward circuit to alleviate NPSCs senescence and disc degeneration.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 2","pages":"Pages 1007-1022"},"PeriodicalIF":14.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Locally producing antibacterial peptide to deplete intratumoral pathogen for preventing metastatic breast cancer

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2025.01.002

Shizhen Geng , Tingting Xiang , Yaru Shi , Mengnian Cao , Danyu Wang , Jing Wang , Xinling Li , Haiwei Song , Zhenzhong Zhang , Jinjin Shi , Junjie Liu , Airong Li , Ke Sun

Metastatic dissemination is the major cause of death from breast-cancer (BC). Fusobacterium nucleatum (F.n) is widely enriched in BC and has recently been identified as one of the high-risk factors for promoting BC metastasis. Here, with an experimental model, we demonstrated that intratumoral F.n induced BC aggressiveness by transcriptionally activating Epithelial-mesenchymal transition-associated genes. Therefore, the F.n may be a potential target to prevent metastasis. Given the fact that cancer-associated fibroblasts (CAFs) are abundant in BC and located near blood vessels, we report an optogenetic system that drives CAF to in situ produce human antibacterial peptide LL37, with the characteristics of biosafety and freely intercellular trafficking, for depleting intratumoral F.n, leading to a 72.1% reduction in lung metastatic nodules number without affecting the balance of the systemic flora. Notably, mild photothermal treatment was found that could normalize CAF, contributing to synergistically inhibiting BC metastasis. In addition, the system can also simultaneously encode a gene of TNF-related apoptosis-inducing ligand to suppress the primary tumor. Together, our study highlights the potential of local elimination of tumor pathogenic bacteria to prevent BC metastasis.

{"title":"Locally producing antibacterial peptide to deplete intratumoral pathogen for preventing metastatic breast cancer","authors":"Shizhen Geng , Tingting Xiang , Yaru Shi , Mengnian Cao , Danyu Wang , Jing Wang , Xinling Li , Haiwei Song , Zhenzhong Zhang , Jinjin Shi , Junjie Liu , Airong Li , Ke Sun","doi":"10.1016/j.apsb.2025.01.002","DOIUrl":"10.1016/j.apsb.2025.01.002","url":null,"abstract":"<div><div>Metastatic dissemination is the major cause of death from breast-cancer (BC). <em>Fusobacterium nucleatum</em> (<em>F.n</em>) is widely enriched in BC and has recently been identified as one of the high-risk factors for promoting BC metastasis. Here, with an experimental model, we demonstrated that intratumoral <em>F.n</em> induced BC aggressiveness by transcriptionally activating Epithelial-mesenchymal transition-associated genes. Therefore, the <em>F.n</em> may be a potential target to prevent metastasis. Given the fact that cancer-associated fibroblasts (CAFs) are abundant in BC and located near blood vessels, we report an optogenetic system that drives CAF to <em>in situ</em> produce human antibacterial peptide LL37, with the characteristics of biosafety and freely intercellular trafficking, for depleting intratumoral <em>F.n</em>, leading to a 72.1% reduction in lung metastatic nodules number without affecting the balance of the systemic flora. Notably, mild photothermal treatment was found that could normalize CAF, contributing to synergistically inhibiting BC metastasis. In addition, the system can also simultaneously encode a gene of TNF-related apoptosis-inducing ligand to suppress the primary tumor. Together, our study highlights the potential of local elimination of tumor pathogenic bacteria to prevent BC metastasis.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 2","pages":"Pages 1084-1097"},"PeriodicalIF":14.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FLZ attenuates Parkinson's disease pathological damage by increasing glycoursodeoxycholic acid production via down-regulating Clostridium innocuum

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.10.011

Meiyu Shang, Jingwen Ning, Caixia Zang, Jingwei Ma, Yang Yang, Yueqi Jiang, Qiuzhu Chen, Yirong Dong, Jinrong Wang, Fangfang Li, Xiuqi Bao, Dan Zhang

Increasing evidence shows that the early lesions of Parkinson's disease (PD) originate from gut, and correction of microbiota dysbiosis is a promising therapy for PD. FLZ is a neuroprotective agent on PD, which has been validated capable of alleviating microbiota dysbiosis in PD mice. However, the detailed mechanisms still need elucidated. Through metabolomics and 16S rRNA analysis, we identified glycoursodeoxycholic acid (GUDCA) was the most affected differential microbial metabolite by FLZ treatment, which was specially and negatively regulated by Clostridium innocuum, a differential microbiota with the strongest correlation to GUDCA production, through inhibiting bile salt hydrolase (BSH) enzyme. The protection of GUDCA on colon and brain were also clarified in PD models, showing that it could activate Nrf2 pathway, further validating that FLZ protected dopaminergic neurons through promoting GUDCA production. Our study uncovered that FLZ improved PD through microbiota–gut–brain axis, and also gave insights into modulation of microbial metabolites may serve as an important strategy for treating PD.

{"title":"FLZ attenuates Parkinson's disease pathological damage by increasing glycoursodeoxycholic acid production via down-regulating Clostridium innocuum","authors":"Meiyu Shang, Jingwen Ning, Caixia Zang, Jingwei Ma, Yang Yang, Yueqi Jiang, Qiuzhu Chen, Yirong Dong, Jinrong Wang, Fangfang Li, Xiuqi Bao, Dan Zhang","doi":"10.1016/j.apsb.2024.10.011","DOIUrl":"10.1016/j.apsb.2024.10.011","url":null,"abstract":"<div><div>Increasing evidence shows that the early lesions of Parkinson's disease (PD) originate from gut, and correction of microbiota dysbiosis is a promising therapy for PD. FLZ is a neuroprotective agent on PD, which has been validated capable of alleviating microbiota dysbiosis in PD mice. However, the detailed mechanisms still need elucidated. Through metabolomics and 16S rRNA analysis, we identified glycoursodeoxycholic acid (GUDCA) was the most affected differential microbial metabolite by FLZ treatment, which was specially and negatively regulated by <em>Clostridium innocuum</em>, a differential microbiota with the strongest correlation to GUDCA production, through inhibiting bile salt hydrolase (BSH) enzyme. The protection of GUDCA on colon and brain were also clarified in PD models, showing that it could activate Nrf2 pathway, further validating that FLZ protected dopaminergic neurons through promoting GUDCA production. Our study uncovered that FLZ improved PD through microbiota–gut–brain axis, and also gave insights into modulation of microbial metabolites may serve as an important strategy for treating PD.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 2","pages":"Pages 973-990"},"PeriodicalIF":14.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Size-transformable nanotherapeutics for cancer therapy

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.11.012

Teng Ma , Tuyen Ba Tran , Ethan Lin , Stephanie Hunt , Riley Haveman , Kylie Castro , Jianqin Lu

The size of nanodrugs plays a crucial role in shaping their chemical and physical characteristics, consequently influencing their therapeutic and diagnostic interactions within biological systems. The optimal size of nanomedicines, whether small or large, offers distinct advantages in disease treatment, creating a dilemma in the selection process. Addressing this challenge, size-transformable nanodrugs have surfaced as a promising solution, as they can be tailored to entail the benefits associated with both small and large nanoparticles. In this review, various strategies are summarized for constructing size-transformable nanosystems with a focus on nanotherapeutic applications in the field of biomedicine. Particularly we highlight recent research developments in cancer therapy. This review aims to inspire researchers to further develop various toolboxes for fabricating size-transformable nanomedicines for improved intervention against diverse human diseases.

纳米药物的大小对其化学和物理特性的形成起着至关重要的作用，从而影响其在生物系统中的治疗和诊断相互作用。纳米药物的最佳尺寸，无论是小尺寸还是大尺寸，在疾病治疗中都具有明显的优势，这就造成了选择过程中的两难问题。为了应对这一挑战，尺寸可变的纳米药物已成为一种前景广阔的解决方案，因为它们可以量身定制，同时具有小尺寸和大尺寸纳米颗粒的优点。本综述总结了构建尺寸可变纳米系统的各种策略，重点关注生物医学领域的纳米治疗应用。我们特别强调了癌症治疗方面的最新研究进展。本综述旨在激励研究人员进一步开发各种工具箱，用于制造尺寸可变的纳米药物，以改善对各种人类疾病的干预。

引用次数: 0

[18F]QTFT, a nicotinate-based radiotracer targeting P2Y12 with satisfactory blood‒brain barrier (BBB) permeability

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2025.02.010

Ying-Qi Song , Chunquan Sheng

引用次数: 0

Nanomaterials evoke pyroptosis boosting cancer immunotherapy

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.11.011

Zhenhua Li, Ziyue Xi, Chuanyong Fan, Xinran Xi, Yao Zhou, Ming Zhao, Lu Xu

Cancer immunotherapy is currently a very promising therapeutic strategy for treating tumors. However, its effectiveness is restricted by insufficient antigenicity and an immunosuppressive tumor microenvironment (ITME). Pyroptosis, a unique form of programmed cell death (PCD), causes cells to swell and rupture, releasing pro-inflammatory factors that can enhance immunogenicity and remodel the ITME. Nanomaterials, with their distinct advantages and different techniques, are increasingly popular, and nanomaterial-based delivery systems demonstrate significant potential to potentiate, enable, and augment pyroptosis. This review summarizes and discusses the emerging field of nanomaterials-induced pyroptosis, focusing on the mechanisms of nanomaterials-induced pyroptosis pathways and strategies to activate or enhance specific pyroptosis. Additionally, we provide perspectives on the development of this field, aiming to accelerate its further clinical transition.

引用次数: 0

Neuronal activities drive brain waste clearance through the glymphatic system

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.11.005

Lin-jian Wang , Xiwen Ma , Jianping Ye

引用次数: 0

Safety, dosimetry, and efficacy of an optimized long-acting somatostatin analog for peptide receptor radionuclide therapy in metastatic neuroendocrine tumors: From preclinical testing to first-in-human study 用于转移性神经内分泌肿瘤肽受体放射性核素治疗的优化长效体生长激素类似物的安全性、剂量和疗效：从临床前试验到首次人体研究

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.05.022

Wei Guo , Xuejun Wen , Yuhang Chen , Tianzhi Zhao , Jia Liu , Yucen Tao , Hao Fu , Hongjian Wang , Weizhi Xu , Yizhen Pang , Liang Zhao , Jingxiong Huang , Pengfei Xu , Zhide Guo , Weibing Miao , Jingjing Zhang , Xiaoyuan Chen , Haojun Chen

Peptide receptor radionuclide therapy (PRRT) with radiolabeled SSTR2 agonists is a treatment option that is highly effective in controlling metastatic and progressive neuroendocrine tumors (NETs). Previous studies have shown that an SSTR2 agonist combined with albumin binding moiety Evans blue (denoted as ¹⁷⁷Lu-EB-TATE) is characterized by a higher tumor uptake and residence time in preclinical models and in patients with metastatic NETs. This study aimed to enhance the in vivo stability, pharmacokinetics, and pharmacodynamics of ¹⁷⁷Lu-EB-TATE by replacing the maleimide-thiol group with a polyethylene glycol chain, resulting in a novel EB conjugated SSTR2-targeting radiopharmaceutical, ¹⁷⁷Lu-LNC1010, for PRRT. In preclinical studies, ¹⁷⁷Lu-LNC1010 exhibited good stability and SSTR2-binding affinity in AR42J tumor cells and enhanced uptake and prolonged retention in AR42J tumor xenografts. Thereafter, we presented the first-in-human dose escalation study of ¹⁷⁷Lu-LNC1010 in patients with advanced/metastatic NETs. ¹⁷⁷Lu-LNC1010 was well-tolerated by all patients, with minor adverse effects, and exhibited significant uptake and prolonged retention in tumor lesions, with higher tumor radiation doses than those of ¹⁷⁷Lu-EB-TATE. Preliminary PRRT efficacy results showed an 83% disease control rate and a 42% overall response rate after two ¹⁷⁷Lu-LNC1010 treatment cycles. These encouraging findings warrant further investigations through multicenter, prospective, and randomized controlled trials.

使用放射性标记的 SSTR2 激动剂的肽受体放射性核素疗法（PRRT）是一种治疗方法，对控制转移性和进展性神经内分泌肿瘤（NET）非常有效。先前的研究表明，SSTR2激动剂与白蛋白结合分子埃文斯蓝（Lu-EB-TATE）结合后，在临床前模型和转移性NETs患者中具有更高的肿瘤摄取率和停留时间。本研究旨在通过用聚乙二醇链取代马来酰亚胺硫醇基团来增强 Lu-EB-TATE 的稳定性、药代动力学和药效学，从而制成一种用于 PRRT 的新型 EB 共轭 SSTR2 靶向放射性药物 Lu-LNC1010。在临床前研究中，Lu-LNC1010 在 AR42J 肿瘤细胞中表现出良好的稳定性和 SSTR2 结合亲和力，在 AR42J 肿瘤异种移植物中的摄取和保留时间也得到了增强。此后，我们公布了 Lu-LNC1010 在晚期/转移性 NET 患者中的首次人体剂量递增研究。所有患者对 Lu-LNC1010 的耐受性良好，不良反应轻微，在肿瘤病灶中的摄取和保留时间长，肿瘤辐射剂量高于 Lu-EB-TATE。初步的 PRRT 疗效结果显示，经过两个 Lu-LNC1010 治疗周期后，疾病控制率为 83%，总体反应率为 42%。这些令人鼓舞的结果值得通过多中心、前瞻性和随机对照试验进行进一步研究。

{"title":"Safety, dosimetry, and efficacy of an optimized long-acting somatostatin analog for peptide receptor radionuclide therapy in metastatic neuroendocrine tumors: From preclinical testing to first-in-human study","authors":"Wei Guo , Xuejun Wen , Yuhang Chen , Tianzhi Zhao , Jia Liu , Yucen Tao , Hao Fu , Hongjian Wang , Weizhi Xu , Yizhen Pang , Liang Zhao , Jingxiong Huang , Pengfei Xu , Zhide Guo , Weibing Miao , Jingjing Zhang , Xiaoyuan Chen , Haojun Chen","doi":"10.1016/j.apsb.2024.05.022","DOIUrl":"10.1016/j.apsb.2024.05.022","url":null,"abstract":"<div><div>Peptide receptor radionuclide therapy (PRRT) with radiolabeled SSTR2 agonists is a treatment option that is highly effective in controlling metastatic and progressive neuroendocrine tumors (NETs). Previous studies have shown that an SSTR2 agonist combined with albumin binding moiety Evans blue (denoted as <sup>177</sup>Lu-EB-TATE) is characterized by a higher tumor uptake and residence time in preclinical models and in patients with metastatic NETs. This study aimed to enhance the <em>in vivo</em> stability, pharmacokinetics, and pharmacodynamics of <sup>177</sup>Lu-EB-TATE by replacing the maleimide-thiol group with a polyethylene glycol chain, resulting in a novel EB conjugated SSTR2-targeting radiopharmaceutical, <sup>177</sup>Lu-LNC1010, for PRRT. In preclinical studies, <sup>177</sup>Lu-LNC1010 exhibited good stability and SSTR2-binding affinity in AR42J tumor cells and enhanced uptake and prolonged retention in AR42J tumor xenografts. Thereafter, we presented the first-in-human dose escalation study of <sup>177</sup>Lu-LNC1010 in patients with advanced/metastatic NETs. <sup>177</sup>Lu-LNC1010 was well-tolerated by all patients, with minor adverse effects, and exhibited significant uptake and prolonged retention in tumor lesions, with higher tumor radiation doses than those of <sup>177</sup>Lu-EB-TATE. Preliminary PRRT efficacy results showed an 83% disease control rate and a 42% overall response rate after two <sup>177</sup>Lu-LNC1010 treatment cycles. These encouraging findings warrant further investigations through multicenter, prospective, and randomized controlled trials.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 2","pages":"Pages 707-721"},"PeriodicalIF":14.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141528599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.11.018

Wei-Qing Deng , Zi-Han Ye , Zhenghai Tang , Xiao-Lei Zhang , Jin-Jian Lu

CD47 is an immune checkpoint widely regarded as a ‘don't eat me’ signal. CD47-based anti-cancer therapy has received considerable attention, with a significant number of clinical trials conducted. While anti-cancer therapies based on CD47 remain a focal point of interest among researchers, it is noteworthy that an increasing number of studies have found that CD47-based therapy ameliorated the pathological status of non-cancer diseases. This review aims to provide an overview of the recent progress in comprehending the role of CD47-based therapy in non-cancer diseases, including diseases of the circulatory system, nervous system, digestive system, and so on. Furthermore, we sought to delineate the promising mechanisms of CD47-based therapy in treating non-cancer diseases. Our findings suggest that CD47-based agents may exert their effect by regulating phagocytosis, regulating T cells, dendritic cells, and neutrophils, and regulating the secretion of cytokines and chemokines. Additionally, we put forward the orientation of further research to bring to light the potential of CD47 and its binding partners as a target in non-cancer diseases.

{"title":"Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases","authors":"Wei-Qing Deng , Zi-Han Ye , Zhenghai Tang , Xiao-Lei Zhang , Jin-Jian Lu","doi":"10.1016/j.apsb.2024.11.018","DOIUrl":"10.1016/j.apsb.2024.11.018","url":null,"abstract":"<div><div>CD47 is an immune checkpoint widely regarded as a ‘don't eat me’ signal. CD47-based anti-cancer therapy has received considerable attention, with a significant number of clinical trials conducted. While anti-cancer therapies based on CD47 remain a focal point of interest among researchers, it is noteworthy that an increasing number of studies have found that CD47-based therapy ameliorated the pathological status of non-cancer diseases. This review aims to provide an overview of the recent progress in comprehending the role of CD47-based therapy in non-cancer diseases, including diseases of the circulatory system, nervous system, digestive system, and so on. Furthermore, we sought to delineate the promising mechanisms of CD47-based therapy in treating non-cancer diseases. Our findings suggest that CD47-based agents may exert their effect by regulating phagocytosis, regulating T cells, dendritic cells, and neutrophils, and regulating the secretion of cytokines and chemokines. Additionally, we put forward the orientation of further research to bring to light the potential of CD47 and its binding partners as a target in non-cancer diseases.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 2","pages":"Pages 757-791"},"PeriodicalIF":14.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oral garlic-derived nanoparticles improve cancer immunotherapy

IF 14.7 1区医学 Q1 PHARMACOLOGY & PHARMACY

Acta Pharmaceutica Sinica. B

Pub Date : 2025-02-01 DOI: 10.1016/j.apsb.2024.12.021

Kun Yang , Jinming Zhang , Bo Xiao

引用次数: 0

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Acta Pharmaceutica Sinica. B

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