Advanced Healthcare Materials
·
2024
·
IF 10
Sijia Wu,Qian Wang,Jun Du,Lejin Zhu,Fujun Yang,Jiacheng Lu,Xueyu Li,Yuhao Li,Jingtao Cui,Yuqing Miao
Sonodynamic therapy (SDT) represents a promising, noninvasive, and precise treatment modality for tumors, demonstrating significant potential in clinical applications. However, the efficiency of sonosensitizers in generating reactive oxygen species (ROS) is often limited by rapid electron-hole recombination. In this study, BiF 3 @BiOI is synthesized via a co-precipitation method, followed by in-situ reduction to decorate it with Pt nanoparticles, resulting in BiF 3 @BiOI@Pt-PVP (BBP) nanocomposite for enhancing SDT efficacy. The formation of the BiF 3 @BiOI heterojunction enhances charge separation ability. The decoration of Pt nanoparticles narrows the bandgap and alters the band positions and Fermi level of BBP, which can effectively mitigate the rapid recombination of electron-hole pairs and facilitate a cascade reaction of ROS, thereby improving ROS generation efficiency with ultrasound excitation. Additionally, bismuth ions in BBP and the generated holes consume glutathione, exacerbating cellular oxidative damage, and triggering PANoptosis and ferroptosis. Furthermore, Pt nanoparticles demonstrate peroxidase-like activity, catalyzing endogenous hydrogen peroxide to oxygen. These functions are helpful against tumors for alleviating hypoxic conditions, reshaping the microenvironment, modulating immune cell infiltration capacity, and enhancing the efficacy of immunotherapy. The dual strategy of forming heterojunctions and sensitization with noble metals effectively enhances the efficacy of sono-catalytic therapy-induced immune activation in tumor treatment.
研究领域:
肿瘤学
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生物材料学
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免疫学
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DOI
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
·
2025
·
IF 3.6
Liu Kan,Tao Tao,Li Ranhong,Wang Huanping,Wang Li,Wu Haiying
Arsenic exposure is well-established to cause neurotoxicity, but its underlying molecular mechanisms remain unclear. This study investigates the effects of early-life arsenic exposure on the nervous system of offspring. Female mice were exposed to NaAsO₂, and alterations in learning, memory, and hippocampal lesions in offspring were assessed. Transcriptome analysis, protein interaction studies, and cellular experiments were integrated to identify key regulatory factors in arsenic-induced neurotoxicity. Arsenic interacts with HUWE1, significantly downregulating its protein expression. HUWE1 inhibition enhances GPX8 stability by reducing its ubiquitination. GPX8 disrupts histone epigenetic modifications by promoting GSH synthesis and arsenic methylation, leading to elevated H3K9 levels. HUWE1 also interacts with KDM3A, and its inhibition reduces KDM3A-mediated H3K9me1/me2 demethylation, amplifying H3K9me2-mediated transcriptional repression of LARS2 and triggering PANoptosis. This study provides novel molecular insights into arsenic-induced neurotoxicity and highlights potential therapeutic targets to mitigate arsenic-related nervous system damage.
研究领域:
毒理学
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神经生物学
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表观遗传学
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分子毒理学
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发育神经科学
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DOI
PubMed
高影响因子
PHYSIOLOGICAL RESEARCH
·
2025
·
IF 2
D Shao,L Bai,Q Chen,Y Chen,Z Qiu,Y Liu,S Jin,Y Wu,J Dai
Trimethylamine N-oxide (TMAO) is involved in the development of kidney disease. However, the specific mechanism by which it leads to kidney injury is unclear. This study explored the role of regulated cell death in TMAO-induced kidney injury. We constructed a TMAO-induced chronic kidney injury model by intraperitoneal injection of TMAO (100 micromol/kg/day for three months). Plasma creatinine (Cre) and urea nitrogen (BUN) levels were measured to evaluate kidney function. Masson staining was used to evaluate kidney pathological changes. The expression levels of regulated cell death-related proteins were measured using western blotting. Plasma Cre and BUN, the area of kidney fibrosis in the TMAO group significantly increased. The western blotting results showed cleaved-Caspase-8, Caspase-8, Caspase-1, NOD-like receptor protein 3 (NLRP3), interleukin-1beta (IL-1beta), cleaved-gasdermin D (cleaved-GSDMD), Z-DNA binding protein 1 (ZBP1), phosphorylation of receptor-interacting protein kinase 3 (RIP3) and mixed-lineage kinase domain-like pseudokinase (MLKL) significantly elevated in the TMAO group. The transferrin receptor 1 (TFR1), ferritin heavy chain (FTH), ferroportin (FPN), nuclear factor erythroid 2-related factor 2 (NRF2), and glutathione peroxidase 4 (GPX4) protein expression in kidney tissue of the TMAO group significantly up-regulated. However, there was no change in iron and MDA levels. The results suggested that PANoptosis, including pyroptosis, apoptosis, and necroptosis components, might be involved in TMAO-induced chronic kidney injury.
研究领域:
肾脏病学
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细胞生物学
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分子生物学
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病理学
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药理学
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DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2023
·
IF 15.1
Rui Zhang,Guobo Chen,Jun Du,Qian Wang,Qingwen Qi,Xueyu Li,Lejin Zhu,Xingzhou Chen,Baolin Liu,Yuqing Miao,Yuhao Li
Photocatalytic therapy (PCT) is a minimally invasive technique that utilizes reactive oxygen species (ROS) to selectively and optically impair tumor cells. However, the limited efficacy of photocatalysts hinders their more comprehensive application. In this study, we successfully synthesized Ce and S-doped Bi 2 O 3 (BOSC) nanosheets through topological synthesis. BOSC exhibits CAT-like and POD-like enzyme activities and can generate ROS and heat upon near-infrared light irradiation, thereby amplifying tumor oxidative stress. Introducing rare earth Ce element enhances light absorption, introduces oxygen vacancies, reduces bandgap, and facilitates charge separation. This Ce-doping also modifies the band position and Fermi level of BOSC, resulting in increased band bending at the solid–liquid interface, enabling a cascade reaction of ROS and enhancing ROS production. Additionally, BOSC demonstrates multiple enzyme activities by depleting GSH and catalyzing the production of ROS and O 2 from endogenous H 2 O 2 , thereby exacerbating cellular oxidative damage. The synergistic effect of BOSC post-illumination induces panoptosis, thereby improving the therapeutic efficacy against tumors. This strategy, involving the modulation of band structure and band bending through ion doping to introduce oxygen defects into the photosensitizer, provides a viable approach to enhance tumor phototherapy.
研究领域:
生物医学
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材料科学
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肿瘤学
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DOI
高影响因子
JOURNAL OF ENVIRONMENTAL MANAGEMENT
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2024
·
IF 8
Meichen Liu,Meichen Gao,Xu Shi,Yilin Yin,Huanyi Liu,Ruirui Xie,Chenxi Huang,Wenwen Zhang,Shiwen Xu
With the increasing development of the society, silicon dioxide (SiO 2 ) has been used in various fields, such as agriculture, food industry, etc., and its residues can pose a potential health threat to organisms. Quercetin (Que) is a potent free radical scavenger commonly found in plants. C57BL/6 mice were chosen to established a mouse model of SiO 2 exposure and Que antagonism to investigate the mechanism of action of Que in rescuing the toxic damage of SiO 2 on mouse cerebellum tissue. The results showed that cytoplasmic vacuolization, and inflammatory cell infiltration caused by SiO 2 were alleviated by the addition of Que, and reduced oxidative stress in mouse cerebellum, alleviated the activation of TLR4 pathway induced by SiO 2 , and substantially reduced the occurrence of ZBP-1-mediated PANoptosis induced by SiO 2 exposure in mouse cerebellum. In NS20Y cells, the oxidative stress activator (Elesclomol) and inhibitor N-acetyl cysteine (NAC), and the NF-κB activator 2 (NA2) were added. Elesclomol and NAC confirm the involvement of ROS in regulating the TLR4/NF-κB pathway, the TLR4/NF-κB pathway regulated ZBP-1-mediated PANoptosis in cerebellum and NS20Y cells induced by SiO 2 exposure. In conclusion, the present experimental data suggest that Que mitigates the onset of ZBP-1-mediated PANoptosis in neuronal cells induced by SiO 2 through the ROS/TLR4/NF-κB pathway. The present experimental findings help to understand the detoxification effect of Que in more tissues and provide an important reference for the rescue of organisms in long-term SiO 2 environment.
研究领域:
神经生物学
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毒理学
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细胞信号传导
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DOI
高影响因子
Science Bulletin
·
2025
·
IF 21.1
Qiang Wang,Yingfei Wen,Bo Bi,Kuan Li,Yuanqi Liu,Binbin Li,Shangbo Zhou,Zihang Li,Jiaqi Xu,Miaojuan Qiu,You Li,Meiying Wu,Yu Chen,Wei Wu,Jing Zhao
Peritoneal metastasis (PM) is typically intractable by immunotherapy due to an immunosuppressive microenvironment and the peritoneal-plasma barrier. Sonodynamic therapy (SDT) presents unique advantages of noninvasive in situ treatment and the potential for antitumor immune activation. Building upon SDT technology, the study reports on a novel biodegradable sonosensitizer, CaS 2 O 8 , characterized by a narrow bandgap, abundant oxygen vacancies and a rapid ultrasound (US) response for abdominal SDT. Such sonosensitizer only produces lethal reactive oxygen species (ROS) after US irradiation, which is nontoxic in a physiological environment. After US irradiation, CaS 2 O 8 yields a large amount of sulfate radical (•SO 4 - ), as well as sonodynamic related ROS (•OH, and 1 O 2 ), which exerts a synergistic effect with Ca 2+ overload to induce Z-conformation nucleic acid by augmenting oxidative damage. As a result, the PANoptosis is initiated through the ZBP1/RIPK3 pathway in tumor cells. This inflammatory cell death leads to a multi-faceted release of tumor cell contents which serve as an in situ tumor antigen to induce a robust antitumor immune response. Notably, the precision sono-immunotherapy enhances the infiltration of T cells into tumors by transforming an immunosuppressive phenotype into an immunostimulatory one. Therefore, targeting PANoptosis by CaS 2 O 8 -induced SDT can provide an alternative or additional clinical treatment and prolonged survival outcome for patients with PM.
研究领域:
肿瘤学
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生物医学工程
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免疫学
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DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2025
·
IF 5.6
Feng Lin,Hong Huang,Jie Long,Renchuan Liang,Yunxi Huang,Xiaoling Luo
Cancer remains a major global health burden due to its high rates of recurrence and resistance to conventional therapies. Although PD-L1/PD-1 immune checkpoint inhibitors (ICIs) have emerged as promising treatments by restoring T cell function and enhancing anti-tumor immunity, their efficacy is often limited by immunosuppressive tumor microenvironment (ITM) and metabolic adaptations that impair T cell activity. To address these challenges, we developed a novel intelligent drug delivery platform that integrates PANoptosis induction, metabolic modulation and targeted nanotherapy. Specifically, hollow mesoporous manganese dioxide (H-MnO 2 ) nanoshells were synthesized and co-loaded with SOAT1 inhibitor avasimibe (Ava). Trop2-specific targeting ligands were further conjugated to enable precise tumor localization, resulting in the multifunctional nanoplatform Ava@HM/Trop2. Upon tumor accumulation via Trop2-mediated targeting, acidic pH conditions and TME stimuli trigger rapid degradation of the H-MnO 2 nanoshells, releasing Ava and inducing PANoptosis. This process activates the cGAS-STING pathway, remodels immunosuppressive TME, mitigates lipid-induced T cell senescence, and synergizes with PD-1 blockade to potentiate anti-tumor immunity. Both in vitro and in vivo experiments demonstrate that Ava@HM/Trop2 achieves efficient tumor targeting, robust tumor cell apoptosis, and improved therapeutic outcomes. This innovative multi-modal strategy highlights a promising avenue for overcoming immunotherapy resistance and advancing the clinical management of solid tumors.
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DOI
PubMed
高影响因子
HUMAN MUTATION
·
2025
·Vol. 2025
·期 1
·5319444
·
IF 3.7
Xin Wu,Linde Sun,Peifa Liu,Qiong Wang,Yu Wang
Background PANoptosis, as an inflammatory programmed cell death, is involved in tumor development. This study set out to discover novel PANoptosis-correlated prognostic signatures in stomach adenocarcinoma (STAD), a prevalent malignancy of the digestive system. Methods STAD samples were derived from a public database, and PANoptosis-related genes (PRGs) were acquired from existing reports. Prognosis-related PRGs were screened by univariate Cox regression analysis. Molecular subtypes of STAD were identified by the “ConsensusClusterPlus” package. The “Limma” package was employed to filter differentially expressed genes (DEGs) between different subtypes. PANoptosis-related prognostic signatures in STAD were identified to establish the RiskScore model. The RiskScore and some of the clinical features were integrated to establish a nomogram. Immune cell infiltration and TIDE score in different risk groups were compared. Correlation between immune checkpoint genes, drug sensitivity, and RiskScore was analyzed by the Spearman method. The biological function of PANoptosis-related signature genes in STAD was preliminarily explored by in vitro cell experiments. Results Based on 18 prognosis-related PRGs, two molecular subtypes of STAD were recognized, and the C1 subtype showed a lower overall survival (OS) rate than the C2 subtype. Further, three PANoptosis-related signature genes ( APOD , GPC3 , and SERPINE1 ) were determined to establish a RiskScore model that could accurately assess the prognostic outcomes for STAD patients. Then, by integrating RiskScore with clinical features, a nomogram was established. The high-risk group had higher immune cell infiltration and TIDE score and lower OS rate than those with a low risk. RiskScore was positively correlated with nine immune checkpoint genes. Besides, we screened 23 drugs that significantly correlated with RiskScore. In vitro cell experiments showed that the mRNA and protein levels of APOD , GPC3 , and SERPINE1 were upregulated in the STAD cell line and that APOD knockout significantly reduced cancer cell proliferation, migration, and invasion levels and increased the apoptotic capacity of the STAD cell line. Conclusion This study established a PANoptosis-related RiskScore model for assessing STAD patient prognosis, which could contribute to the personalized treatment of STAD.
研究领域:
肿瘤学
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分子生物学
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生物信息学
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免疫治疗
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精准医学
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DOI
PubMed
高影响因子
Journal of Neuroinflammation
·
2024
·Vol. 21
·期 1
·1-25
·
IF 9.3
Cheng Shimei,Lu Qiying,Liu Qiuli,Ma Yuanchen,Chen Jinshuo,Lu Di,Huang Mudan,Huang Yinong,Zhao Erming,Luo Jing,Zheng Haiqing
Background Neuronal death is the primary cause of poor outcomes in cerebral ischemia. The inflammatory infiltration in the early phase of ischemic stroke plays a vital role in triggering neuronal death. Either transplantation of mesenchymal stem cells (MSCs) derived from humans or repetitive transcranial magnetic stimulation (rTMS) have respectively proved to be neuroprotective and anti-inflammatory in cerebral ischemia. However, either treatment above has its limitations. Whether these two therapies have synergistic effects on improving neurological function and the underlying mechanisms remains unclear. This investigation aims to elucidate the synergistic effects and underlying mechanisms of MSCs combined with rTMS treatment on the neurological function recovery post-ischemia.Methods A Sprague-Dawley rat model of cerebral infarction was induced via transient middle cerebral artery occlusion (tMCAO). The rats were divided into five groups (n = 50): sham, tMCAO, rTMS, MSCs, and MSCs + rTMS groups. Transplantation of human umbilical cord MSCs and rTMS intervention were performed 24 h post-stroke. Neurological function was further assessed via several behavioral tests and the 2,3,5-triphenyltetrazolium chloride (TTC) staining companied with Nissl staining were used to assess neuronal survival. TUNEL staining, western blotting, immunofluorescence, immunohistochemistry, ELISA, and flow cytometry were employed to measure the levels of neuroinflammation and PANoptosis. The molecular mechanisms underlying the special role of rTMS in the combined therapy were distinguished with transcriptome sequencing via PC12 cells in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions.Results The combined therapy efficiently reduced lesion volume and improved neuronal survival (P < 0.05), subsequently improving functional recovery after ischemic stroke. MSCs + rTMS treatment ameliorated the PANoptosis in neurons (P < 0.05), accompanied by decreased levels of inflammatory factors in the cerebral tissue and serum during the subacute phase of cerebral infarction. To further explore the roles of either therapy on synergistic effect, we found that the transplanted MSCs primarily localized in the spleen and reduced cerebral inflammatory infiltration after ischemia via suppressed splenic inflammation. Meanwhile, rTMS significantly protects neurons from PANoptosis in MSCs-inhibited inflammatory conditions by downregulating REST unveiled by transcriptome sequencing.Conclusion sOur study elucidates an unidentified mechanism by which the combination of MSCs and rTMS could synergistically promote neuronal survival and suppress neuroinflammation during the subacute phase of cerebral infarction, thus improving neurological outcomes. The downregulating REST induced by rTMS may potentially contribute to the neuroprotective effect against PANoptosis in MSCs-inhibited inflammatory conditions. These results are expected to provide novel insights into the mechanisms of MSCs and rTMS combination therapy in synergistically protecting against cerebral ischemia injury and potential targets underlying neuronal PANoptosis in the early phase of stroke.
研究领域:
神经科学
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干细胞生物学
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神经病学
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免疫学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ACTA PHARMACOLOGICA SINICA
·
2024
·
IF 6.9
You Yi-ping,Yan Liang,Ke Hua-yu,Li Ya-ping,Shi Zi-jian,Zhou Zhi-ya,Yang Hai-yan,Yuan Tao,Gan Ying-qing,Lu Na,Xu Li-hui,Hu Bo,Ou-Yang Dong-yun,Zha Qing-bing,He Xian-hui
PANoptosis is an emerging form of regulated cell death (RCD) characterized by simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling that not only participates in pathologies of inflammatory diseases but also has a critical role against pathogenic infections. Targeting PANoptosis represents a promising therapeutic strategy for related inflammatory diseases, but identification of inhibitors for PANoptosis remains an unmet demand. Baicalin (黄芩苷) is an active flavonoid isolated from Scutellaria baicalensis Georgi (Huangqin), a traditional Chinese medicinal herb used for heat-clearing and detoxifying. Numerous studies suggest that baicalin possesses inhibitory activities on various forms of RCD including apoptosis/secondary necrosis, pyroptosis, and necroptosis, thereby mitigating inflammatory responses. In this study we investigated the effects of baicalin on PANoptosis in macrophage cellular models. Primary macrophages (BMDMs) or J774A.1 macrophage cells were treated with 5Z-7-oxozeaenol (OXO, an inhibitor for TAK1) in combination with TNF-α or LPS. We showed that OXO plus TNF-α or LPS induced robust lytic cell death, which was dose-dependently inhibited by baicalin (50−200 μM). We demonstrated that PANoptosis induction was accompanied by overt mitochondrial injury, mitochondrial DNA (mtDNA) release and Z-DNA formation. Z-DNA was formed from cytosolic oxidized mtDNA. Both oxidized mtDNA and mitochondrial Z-DNA puncta were co-localized with the PANoptosome (including ZBP1, RIPK3, ASC, and caspase-8), a platform for mediating PANoptosis. Intriguingly, baicalin not only prevented mitochondrial injury but also blocked mtDNA release, Z-DNA formation and PANoptosome assembly. Knockdown of ZBP1 markedly decreased PANoptotic cell death. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), administration of baicalin (200 mg/kg, i.g., for 4 times) significantly mitigated lung and liver injury and reduced levels of serum TNF-α and IFN-γ, concomitant with decreased levels of PANoptosis hallmarks in these organs. Baicalin also abrogated the hallmarks of PANoptosis in liver-resident macrophages (Kupffer cells) in HLH mice. Collectively, our results demonstrate that baicalin inhibits PANoptosis in macrophages by blocking mitochondrial Z-DNA formation and ZBP1-PANoptosome assembly, thus conferring protection against inflammatory diseases. PANoptosis is a form of regulated cell death displaying simultaneous activation of pyroptotic, apoptotic, and necroptotic signaling. This study shows that induction of PANoptosis is linked to mitochondrial dysfunction and mitochondrial Z-DNA formation. Baicalin inhibits PANoptosis in macrophages in vitro via blocking mitochondrial dysfunction and the mitochondrial Z-DNA formation and thereby impeding the assembly of ZBP1-associated PANoptosome. In a mouse model of hemophagocytic lymphohistiocytosis (HLH), baicalin inhibits the activation of PANoptotic signaling in liver-resident macrophages (Kupffer cells) in vivo, thus mitigating systemic inflammation and multiple organ injury in mice.
研究领域:
免疫学
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细胞生物学
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药理学
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炎症
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调控性细胞死亡
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DOI
PubMed
高影响因子
BIOMATERIALS
·
2025
·
IF 12.9
Silin Du,Guangyu Ma,Xiang Li,Minghao Chao,Liying Fan,Zhiqiang Zhao,Rongze Tang,Junjie Li,Chaonan Jing,Yufan Liu,Dehong Yu,Zhao Liu,Fenglei Gao
To overcome the resistance of tumor cells to death through a single pathway, PANoptosis, a novel synergistic mode of cell death, can simultaneously activates pyroptosis, apoptosis, and necroptosis. Most current strategies for inducing PANoptosis focused on amplifying reactive oxygen species (ROS) through exogenous stimuli, while the regulatory role of tumor cell metabolic characteristic in this process has long been overlooked. We propose a ROS-Metabolism dual axis synergistic induction of PANoptosis, simultaneously enhancing antitumor immune responses, and construct a novel bionic nanoplatform named CVOVM. This platform consists of CoVO x nanocakes and the glutamine transporter inhibitor V-9302, with 4T1 cell membranes as camouflage. In tumors, CVOVM initiates a series of catalytic reactions: CoVO x promotes numerous ROS generation, while V-9302 disrupts glutamine metabolism, depleting glutathione (GSH) and nicotinamide adenine dinucleotide (NAD + ), thereby triggering the assembly of PANoptosome primarily composed of NLRP3 and NLRC5, which initiates pyroptosis, apoptosis, and necroptosis. The occurrence of PANoptosis promotes immunogenic cell death (ICD) to remodel tumor immunosuppressive microenvironment, and enhances immunotherapy and inhibits lung metastasis. Overall, we present a previously unreported mechanis to achieve the synergistic induction of PANoptosis through ROS amplification and metabolic inhibition, enhancing antitumor immunity, and potentially providing new opportunities and possibilities for combination cancer therapy.
研究领域:
癌症研究
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纳米医学
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免疫治疗
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细胞死亡机制
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活性氧信号通路
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肿瘤代谢
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仿生纳米材料
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DOI
PubMed
高影响因子
Science Bulletin
·
2026
·
IF 21.1
Xinran Song,Xinyue Dai,Hui Huang,Lili Xia,Chengyao Wu,Yu Chen
The rapid progress of interdisciplinary medicine has significantly boosted ultrasound-based therapeutic modalities and strategies. The sonosensitizers, as core components of traditional sonodynamic therapy, have drawn escalating research focus for their unique therapeutic performance, but their clinical translation remains severely hampered by critical bottlenecks of biodegradability, required semiconductor characteristic, and long-term biosafety risks, which underscore an urgent demand for innovative sonosensitizers coupled with breakthrough therapeutic modalities to revolutionize ultrasound-based therapeutics. Herein, we strategically engineered the optimized iron oxyhydroxide nanorods as a high-performance ultrasound-activated sono-tribocatalytic nanosystem for efficient sono-tribocatalytic therapy (STT). This sono-tribocatalytic sonosensitizer demonstrates exceptional tribocatalytic efficacy in radical generation while maintaining excellent recyclability. Its mechanism originates from the surface charges on sonosensitizers generated by tribocatalysis that interact with dissolved oxygen and hydroxyl species, which generate reactive oxygen species to drive redox reactions. Crucially, the accumulated cytotoxic hydroxyl and superoxide radicals induce simultaneous mitochondrial dysfunction and redox homeostasis disruption in cancer cells, triggering specific PANoptosis. The in vivo assessments validate its potent antineoplastic effect. It achieves remarkable tumor inhibition through mechano-chemical activation by the intrinsic STT mechanism. This study establishes the first STT paradigm capable of inducing PANoptosis for efficient cancer treatment, thereby significantly expanding the application scope of sonocatalytic medicine to diverse disease interventions.
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高影响因子
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