Cell Death & Disease最新文献

{"title":"Retraction Note: Histone acetyltransferase PCAF accelerates apoptosis by repressing a GLI1/BCL2/BAX axis in hepatocellular carcinoma.","authors":"X Gai, K Tu, C Li, Z Lu, L R Roberts, X Zheng","doi":"10.1038/s41419-026-09338-0","DOIUrl":"10.1038/s41419-026-09338-0","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer.","authors":"T Yu, T-D Shan, J-Y Li, C-Z Huang, S-Y Wang, H Ouyang, X-J Lu, J-H Xu, W Zhong, Q-K Chen","doi":"10.1038/s41419-026-09339-z","DOIUrl":"https://doi.org/10.1038/s41419-026-09339-z","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-3 restrains T cell-driven inflammation in the testis and epididymis.","authors":"Hiba Hasan, Kimberly Jandel, Eva Wahle, Gabriela Michel, Linda Kreyling, Vishnu Kumar, Tara Procida-Kowalski, Sudhanshu Bhushan, Michaela Frolikova, Jens Rosellen, Thorsten Diemer, Katerina Komrskova, Marek Bartkuhn, Martin Speckmann, Hans-Christian Schuppe, Daniela Fietz, Christiane Pleuger, Andreas Meinhardt, Monika Fijak","doi":"10.1038/s41419-026-09304-w","DOIUrl":"10.1038/s41419-026-09304-w","url":null,"abstract":"<p><p>Galectin-3 (Gal-3) is a pleiotropic molecule involved in immune regulation and tissue homeostasis. While it has been implicated in reproductive tissue function, its role in shaping immune cell dynamics within the testis and epididymis remains incompletely defined. Here, we investigated the function of Gal-3 in the testis and epididymis under steady-state and inflammatory conditions, to determine its contribution to inflammatory responses and tissue damage. In both murine and human tissues, Gal-3 frequency and staining intensity increased along the testicular-epididymal axis, with the highest proportion of Gal-3⁺ cells in the cauda epididymidis, where it was detected across multiple murine immune cell populations, as well as epithelial and germ cells. Consistent with this distribution, Gal-3 deficiency reshaped the local immune landscape, leading to reduced macrophage populations and increased T cell abundance in the testis and cauda epididymidis. In a model of experimental autoimmune epididymo-orchitis (EAEO), Gal-3-deficient (Lgals3^-/-) mice exhibited exacerbated inflammation, fibrosis, and irreversible organ damage, accompanied by increased T cell frequencies among CD45⁺ cells. Transcriptomic analysis revealed enhanced T cell activation signatures, particularly involving IFN-γ-related pathways. Functionally, Gal-3-deficient T cells showed increased cytokine production, specifically IFN-γ, which was further amplified in the presence of Gal-3-deficient macrophages, which in turn acquired a pro-inflammatory phenotype. Together, these findings identify Gal-3 as a key regulator of T cell activity and macrophage polarization with prominent effects in the testis and epididymis, with implications for understanding immune-mediated infertility.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial Expression of Concern: The bromodomain and extra-terminal inhibitor CPI203 enhances the antiproliferative effects of rapamycin on human neuroendocrine tumors.","authors":"C Wong, S V Laddha, L Tang, E Vosburgh, A J Levine, E Normant, P Sandy, C R Harris, C S Chan, E Y Xu","doi":"10.1038/s41419-026-09313-9","DOIUrl":"10.1038/s41419-026-09313-9","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13614922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cuproptosis in iron overload hepatocytes.","authors":"Judith Sailer, Jonas Gottal, Leon Kaub, Adrian T Jauch, Jonas Engler, Carola Eberhagen, Christine von Toerne, Lea Hansen-Palmus, Valerie Wachinger, Banu Akdogan, Stefan Engelhardt, Percy Knolle, Alan A DiSpirito, Ulrike Protzer, Maja Vujić Spasić, Hans Zischka","doi":"10.1038/s41419-026-09275-y","DOIUrl":"10.1038/s41419-026-09275-y","url":null,"abstract":"<p><p>A long-standing clinical conundrum is the pronounced phenotypic heterogeneity of hereditary hemochromatosis. Patients with identical HFE genotypes and similar degrees of iron overload can have vastly different clinical outcomes, ranging from being completely asymptomatic to developing severe cirrhosis, diabetes, or cardiomyopathy. This variability strongly implies the existence of genetic or environmental modifiers that dictate disease penetrance. Here, copper may be a compelling disease-modifying candidate, due to its intimately intertwined metabolism with iron. Indeed, profound iron loading in hemochromatosis mice (Hfe knockout) and hemochromatosis Huh7 hepatocytes does not cause overt toxicity. However, the addition of copper, even in trace amounts and harmless on its own, dramatically amplifies adverse effects to induce profound cell toxicity. We find that copper-provoked iron vulnerability is not driven by Fenton chemistry-driven ROS damage, but instead induces a cuproptotic-like mechanism, characterized by proteotoxic stress, loss of iron-sulfur cluster enzyme activity, and severe mitochondrial dysfunction. Remarkably, high-affinity copper chelation rescued Huh7 cells, whereas inhibition of other canonical cell death pathways did not. These findings spotlight copper as a critical modifier in iron overload toxicity, capable of converting largely compensated iron overload into severe cellular injury and death, thereby providing a mechanistic explanation for the phenotypic heterogeneity in hemochromatosis.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MIC13-linked cristae disruption causes metabolic failure and early fibrotic remodelling in mitochondrial liver disease.","authors":"Alexander Becker, Thomas O Eichmann, Viacheslav Vasiliev, Kira An Mey, Patrick Petzsch, Andrea Rossi, Felix Distelmaier, Ruchika Anand","doi":"10.1038/s41419-026-09283-y","DOIUrl":"10.1038/s41419-026-09283-y","url":null,"abstract":"<p><p>Mitochondrial diseases are highly complex and heterogeneous, and nearly 20% of cases involve severe liver pathology. Here, we report an affected individual carrying a pathogenic MIC13 variant (c.260-2 A > G) associated with early-onset mitochondrial hepato-encephalopathy. Such mitochondrial hepatopathies are rare, multisystemic disorders with major liver involvement, difficult to diagnose, lack effective treatment, and are poorly understood, in part due to the absence of faithful disease-relevant cellular models. To investigate hepatocyte-specific consequences of the MIC13 variant, we generated iPSCs carrying this disease-causing variant and differentiated them into induced hepatocytes (iHeps). MIC13, a key component of the MICOS complex required for cristae formation, was disrupted in these cells, and the resultant iHeps exhibited the same cristae defects observed in clinical samples. Integrated multi-omics and biochemical analyses revealed extensive metabolic rewiring, including disrupted amino acid turnover, accumulation of tricarboxylic acid (TCA) and urea cycle intermediates. Additionally, profound alterations in methionine cycle and transsulfuration pathways, along with enhanced bile acid synthesis, collectively affect methylation potential, redox homeostasis, and detoxification. Lipid metabolism was also impaired, with incomplete β-oxidation, increased ketogenesis, and diminished lipid storage. At the cellular level, extensive extracellular matrix (ECM) remodeling, increased intracellular collagen accumulation and enhanced cell migration indicated an early fibrotic phenotype, linking metabolic rewiring to ECM homeostasis. Overall, this clinically relevant model uncovers how cristae defects drive metabolic imbalance and hepatocyte dysfunction, ultimately leading to early fibrotic changes in mitochondrial liver disease. These findings provide a strong mechanistic foundation for understanding mitochondrial liver disease and developing targeted therapeutic strategies.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13578304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PGC-1α and PPARs cooperatively mediate photoreceptor neuroprotection in rd1 mouse inherited retinal degeneration.","authors":"Lan Wang, Jie Yan, Javier Sancho-Pelluz, Qianlu Yang, Zhulin Hu, Kangwei Jiao, Mathias W Seeliger, François Paquet-Durand","doi":"10.1038/s41419-026-09254-3","DOIUrl":"10.1038/s41419-026-09254-3","url":null,"abstract":"<p><p>Retinitis pigmentosa (RP) is a group of inherited diseases characterized by primary rod photoreceptor dysfunction and progressive cone cell death. Due to their very high energy demand, the degeneration of photoreceptors may be linked to insufficient energy supply or metabolic imbalance. Critical transcription factors that regulate metabolism, such as peroxisome proliferator-activated receptors (PPARs) and PPAR gamma coactivator 1α (PGC-1α), have been found to play important roles in neurodegenerative diseases, but their potential roles in RP have yet not been elucidated. Here, organotypic retinal explant cultures derived from retinal degeneration 1 (rd1) mice were used to investigate the effects of PPARα, PPARγ, PPARβ/δ agonists, as well as PGC-1α activation and inhibition. Photoreceptor death was quantified using the TUNEL assay, while in situ activity assays were used to monitor effects of PPARs and PGC-1α on poly (ADP-ribose) polymerase (PARP) and calpain activity. Generation of poly (ADP-ribose) (PAR) and activation of calpain-1 and calpain-2 were evaluated by immunostaining. PGC-1α/PPAR-associated transcriptional changes were assessed by RT-qPCR. We found that PPARβ/δ agonists had limited effects, while treatment targeting PPARα, PPARγ, and PGC-1α significantly reduced photoreceptor death and PARP activity in rd1 retina. RT-qPCR analysis in treated rd1 retina confirmed upregulation of genes downstream of PGC-1α/PPAR signaling. Stimulation of the histone deacetylase sirtuin-1, an upstream regulator of PGC-1α, had no beneficial effect on photoreceptor viability unless combined with PARP inhibition. Furthermore, PPARγ and PGC-1α effectively suppressed overall calpain activity and overactivation of calpain-2, alleviating photoreceptor degeneration caused by Ca²⁺ imbalance. In summary, our data support the concept of a PARP-sirtuin-1-PGC-1α-PPAR-PARP feedback control that connects defective energy metabolism to photoreceptor degeneration. Specifically, our findings suggest that PPARα, PPARγ, and PGC-1α cooperate to preserve photoreceptor viability, highlighting PPAR-signaling as a promising target for future therapeutic interventions.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13575171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Westernized diet related arachidonic acid metabolism expands DNA error-prone growth factor-dependent colonic quiescent stem cells in adolescent mice.","authors":"Lea Christiansen, Mohab Ragab, Laura Nickel, Annika Sünderhauf, Lina Jegodzinski, Maren Hicken, Heidi Schlichting, Rudrik Weikamp, Franziska Schmelter, Daniel Margis, Stefan Mertel, Ines Richerzhagen, Henrike Wenk, Luise Pötter, Sebastian Tornow, Nele Buchmann, Daniel Vondran, Clarissa Gottschild, Annika Raschdorf, Larissa Nogueira de Almeida, Axel Künstner, Hauke Busch, Timo Gemoll, Christian D Sadik, Darko Castven, Jens U Marquardt, Senad Divanovic, Walter Raasch, Christian Sina, Stefanie Derer","doi":"10.1038/s41419-026-09240-9","DOIUrl":"10.1038/s41419-026-09240-9","url":null,"abstract":"<p><p>Given the association between early-onset colorectal cancer (eoCRC) and insulin resistance (IR), we investigated the effects of westernized diet (WD)-induced IR on intestinal stem cells (ISCs) by in-depth phenotyping three adolescent mouse models of escalating WD-driven IR. WD-related hyperlipidaemia and hyperglycaemia enhanced ω6-polyunsaturated fatty acid (PUFA) metabolism, while inhibiting glucose metabolism, resulting in colonic epithelial cell (EC) energy deficiency, hypoproliferation, and quiescent ISCs (qISC) expansion. WD-induced systemic IR provoked colonic EC IR, reduced ω6-PUFA metabolism, which was compensated by aberrated triglyceride metabolism and growth factor receptor signalling, causing hyperproliferation of expanded qISCs. Combined with single-cell transcriptomic data and colonic 3D-organoid analysis we revealed that the ω6-PUFA arachidonic acid inhibited glucose uptake, favouring colonic EC IR driven expansion of the lipid-dependent inherently DNA-mismatch prone qISC compartment in expense of the insulin-dependent LGR5⁺ ISCs. Overall, our findings may open new alleys for targeted nutritional interventions in eoCRC prevention.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13575188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A pro-inflammatory metastasis-associated macrophage subset induces tumor-promoting mesothelial cell conversion in ovarian cancer via IL-1α secretion.","authors":"Sophie Heidemann, Florian Finkernagel, Anna Mary Steitz, Julie Koennecke, Franziska Werner, Vanessa M Beutgen, Witold Szymanski, Johannes Graumann, Julia Teply-Szymanski, Andrea Nist, Thorsten Stiewe, Corinna U Keber, Niklas Gremke, Uwe Wagner, Carsten Denkert, María Gómez-Serrano, Elke Pogge von Strandmann, Rolf Müller, Silke Reinartz","doi":"10.1038/s41419-026-09280-1","DOIUrl":"10.1038/s41419-026-09280-1","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) are key regulators of the tumor microenvironment, yet the functional specialization of TAM subsets in metastatic progression remains incompletely defined. Here, we characterized distinct TAM populations contributing to tumor-promoting mesothelial cell conversion in high-grade ovarian carcinoma using single-cell RNA sequencing of patient-derived macrophages from ascites (ascTAMs) and omental metastases (omTAMs). TAMs from these anatomical sites were clearly distinguishable by polarization states, with omTAMs exhibiting a mixed M1⁺/M2⁺ phenotype, in contrast to the M1^low/M2⁺ profile observed in ascTAMs. Transcriptomic analysis further revealed functional divergence of these subsets. Notably, omTAMs displayed gene signatures associated with mesothelial-to-mesenchymal transition (MMT), a critical process enabling tumor invasion across the peritoneal lining. Functionally, conditioned media from omTAMs, similar to that from classically activated M1 macrophages, induced MMT in primary mesothelial cells via TGFβ and ERK/p38 MAPK signaling pathways. This phenotypic transition enhanced transmesothelial tumor cell invasion. Proteomic analysis identified IL-1α as a key MMT-inducing factor secreted by pro-inflammatory macrophages. Mechanistically, IL-1α cooperates with TGFβ by activating an autocrine TGFβ/TGFBR1 feedback loop in mesothelial cells, thereby amplifying MMT. Consistent with these findings, IL1A expression was enriched in omTAM clusters across independent patient samples and was confirmed by immunohistochemical analysis of clinical samples. From a therapeutic perspective, our study identifies new avenues to counteract the mesothelial reprogramming driven by IL-1α⁺ TAMs, potentially impeding metastatic progression. Created in BioRender. Heidemann, S. (2026) https://BioRender.com/aeu6yd0 .</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SUMOylated Reptin maintains low intracellular ROS levels by activating mitophagy to drive gemcitabine resistance in gallbladder cancer.","authors":"Chuanxin Yang, Wei Wang, Yaodi Shao, Xiangjun Wang, Yangming Liu, Liqin Yu, Sijie Zhang, Renhao Xue, Jian Wang","doi":"10.1038/s41419-026-08598-0","DOIUrl":"10.1038/s41419-026-08598-0","url":null,"abstract":"<p><p>Gemcitabine resistance remains a major challenge in the treatment of gallbladder cancer (GBC). Here, we elucidate a novel mechanism underlying gemcitabine resistance in GBC, centered on a self-reinforcing mitophagy/ROS/SENP3/Reptin loop. Gemcitabine-resistant GBC cells maintain significantly lower intracellular reactive oxygen species (ROS) levels than wild-type cells through enhanced mitophagy. This finding delineates a novel transcriptional mechanism that drives mitophagy under low ROS conditions. Mechanistically, this low ROS state decreases the protein abundance of the ROS sensor Sentrin/SUMO-specific protease 3 (SENP3), thereby promoting SUMOylation of its substrate, RuvB-like AAA+ ATPase 2 (Reptin), at the K456 site. SUMOylated Reptin translocates to the nucleus, where it acts as a transcriptional activator to specifically upregulate PTEN-induced putative kinase 1 (PINK1), a key mitophagy regulator. Enhanced PINK1 expression further amplifies mitophagy, effectively scavenging ROS and perpetuating the low ROS state that drives resistance, thus sustaining the gemcitabine-resistant phenotype. Clinically, low SENP3 expression and high Reptin expression correlate with poor gemcitabine response and shorter overall survival in GBC patients. Targeting this pathway, the Reptin ATPase inhibitor CB-6644 effectively suppressed PINK1 transcription, inhibited mitophagy, increased ROS accumulation, and reversed gemcitabine resistance both in vitro and in vivo. These findings identify the mitophagy/ROS/SENP3/Reptin loop as a core resistance mechanism in GBC, highlight SENP3 and Reptin as predictive biomarkers, and establish CB-6644 as a promising therapeutic agent to overcome gemcitabine resistance by disrupting this adaptive pathway.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}