Prostaglandins & other lipid mediators最新文献

{"title":"Spatial remodeling of the sphingolipid rheostat in colorectal carcinogenesis.","authors":"Anna J Sadowska, Adam R Markowski","doi":"10.1016/j.prostaglandins.2026.107105","DOIUrl":"10.1016/j.prostaglandins.2026.107105","url":null,"abstract":"<p><p>Colorectal carcinogenesis involves coordinated reorganization of epithelial architecture, metabolism, and microenvironmental interactions. Among lipid signaling pathways, the sphingolipid rheostat has traditionally been described as a balance between ceramides and sphingosine-1-phosphate (S1P), with opposite effects on cell death and survival. However, current evidence suggests that this model is too simplified for colorectal cancer. Here, we discuss the sphingolipid rheostat as a spatially organized and stage-dependent signaling network shaped by enzymatic control, lipid transport, extracellular carrier association, and receptor context. During adenoma formation, ceramide-related metabolic programs may support progenitor cell function, while luminal ceramide generation by alkaline sphingomyelinase provides a surface-associated checkpoint linked to epithelial turnover. In carcinomas, coordinated rewiring of multiple regulatory nodes, including increased S1P synthesis, reduced degradation, altered export, and diversion of ceramide into complex sphingolipids, appears to favor persistent pro-survival signaling. These changes are associated with apoptosis resistance, angiogenesis, invasion, and immune modulation. We further emphasize that sphingolipid signaling depends on exposure biology, including cellular source, transporter usage, and carrier distribution in the circulation. This framework may help explain why blood-based sphingolipid measurements do not always reflect tumor-local sphingolipid organization. A compartment-aware view of sphingolipid biology may therefore improve interpretation of lipid biomarkers and identify stage-specific therapeutic vulnerabilities.</p>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":" ","pages":"107105"},"PeriodicalIF":2.6,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibiotic-induced disruption of lipid mediator signaling: Implications for cardiovascular inflammation and cardiotoxicity.","authors":"Rahul Jaiswal, Tarique Mahmood, Himani Awasthi, Farogh Ahsan, Asad Ali","doi":"10.1016/j.prostaglandins.2026.107103","DOIUrl":"10.1016/j.prostaglandins.2026.107103","url":null,"abstract":"<p><p>Antibiotics remain the cornerstone of treatment for infectious disease, yet a growing body of evidence shows that these drugs also disrupt host inflammatory and metabolic pathways well beyond their intended antimicrobial target. One consequence that has received comparatively little attention is their effect on lipid mediator signaling. Polyunsaturated fatty acids serve as precursors to lipid mediators that keep the vasculature in balance by governing both inflammatory and resolving pathways. Antibiotic exposure disturbs this balance in two connected ways, by driving gut microbiota dysbiosis and by directly impairing mitochondrial function and raising oxidative stress. Together these changes tilt lipid mediator profiles toward pro-inflammatory eicosanoids at the expense of pro-resolving mediators, promoting endothelial dysfunction, atherosclerosis progression, and myocardial injury. This review brings together the laboratory and clinical evidence linking antibiotic use to lipid mediator disturbances and cardiovascular risk, and considers strategies that may help preserve lipid mediator balance during antibiotic therapy.</p>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":" ","pages":"107103"},"PeriodicalIF":2.6,"publicationDate":"2026-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Effects of aged garlic extract on blood pressure in hypertensive patients: A systematic review and meta-analysis of randomized controlled trials\" [PRO 175 (2024) 106914].","authors":"Mohamed J Saadh, Muthena Kariem, Madhu Shukla, Suhas Ballal, Abhishek Kumar, Mamata Chahar, Suman Saini, Ish Kapila, Shirin Hasaanzadeh","doi":"10.1016/j.prostaglandins.2026.107100","DOIUrl":"10.1016/j.prostaglandins.2026.107100","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":" ","pages":"107100"},"PeriodicalIF":2.6,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NPY deficiency protects against osteoporosis by altering bone lipid metabolism","authors":"Hanshi Wang,&nbsp;Jiaxiang Huang,&nbsp;Yuxun Lv,&nbsp;Jiansheng Deng,&nbsp;Hui Ye,&nbsp;Jin Chen","doi":"10.1016/j.prostaglandins.2026.107088","DOIUrl":"10.1016/j.prostaglandins.2026.107088","url":null,"abstract":"<div><h3>Background</h3><div>Osteoporosis is a major global health issue characterized by imbalanced bone remodeling. Neuropeptide Y (NPY) is a key regulator of energy metabolism and bone homeostasis, but its role in osteoporosis progression remains poorly defined.</div></div><div><h3>Methods</h3><div>This study enrolled 74 participants, including 38 osteoporosis patients and 36 controls, and evaluated the relationship of NPY levels with other clinical indicators. NPY knockout and wild-type mice with or without ovariectomy were used to investigate the role of NPY in bone loss and changes in the bone lipid profile. Bone loss was assessed by micro-computed tomography. Tissue lipidomic analysis was performed by liquid chromatography mass spectrometry.</div></div><div><h3>Results</h3><div>The serum NPY levels of female patients with osteoporosis were significantly elevated compared with the corresponding control group. In female patients, lumbar spine T-score, spin T-score and vitamin D level showed significant negative correlation with NPY level. NPY knockdown protected against ovariectomy-induced bone loss, and their lipids in bone were profiled. As many as 18 lipids classes were quantified, and overall levels of phosphatidylinositol and lysophosphatidyl choline were greatly changed with NPY silence. In detail, 49 lipids were significantly altered due to NPY in OVX mice, 12 of which were related to osteoporosis. Interestingly, TAG was the main component among them, and it indicated some specific TAG could be connected with NPY on osteoporosis.</div></div><div><h3>Conclusions</h3><div>NPY ablation protects against osteoporosis by altering bone lipid metabolism. Therefore, NPY could be a potential target for osteoporosis treatment.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"185 ","pages":"Article 107088"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148309362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lack of association between the Cytochrome P450 4F2 rs2108622 genotype and responses to valsartan and amlodipine among a sample of Jordanian hypertensive patients","authors":"Yazun Bashir Jarrar,&nbsp;Enas Yousef Alkasasbeh,&nbsp;Dalia Abdelrazaq,&nbsp;Wiam Khalil,&nbsp;Malek Zihlif,&nbsp;Hussein Alhawari,&nbsp;Sireen Abdul Rahim Shilbayeh","doi":"10.1016/j.prostaglandins.2026.107091","DOIUrl":"10.1016/j.prostaglandins.2026.107091","url":null,"abstract":"<div><h3>Background</h3><div>The <em>Cytochrome 4F2 (CYP4F2) rs2108622</em> genetic variant influences the production of 20-Hydroxyeicosatetraenoic acid (20-HETE), which affects the blood pressure. Previous findings from our group indicate that <em>CYP4F2 rs2108622</em> genotype is associated with essential hypertension.</div></div><div><h3>Aims</h3><div>This study aims to find out the association of <em>CYP4F2 rs2108622</em> genotype with the response of valsartan and amlodipine among hypertensive patients.</div></div><div><h3>Methods</h3><div>56 hypertensive patients on 80 mg valsartan and 34 on 5 mg amlodipine were genotyped for <em>CYP4F2 rs2108622</em> genetic variant using PCR-RFLP method. The systolic (SBP) and diastolic (DBP) blood pressures data before and after one month antihypertensive treatment were collected from the computer record of the hospital. The patients were unrelated Arabs attending the University of Jordan Hospital.</div></div><div><h3>Results</h3><div>We found that carriers of <em>CYP4F2 rs2108622 CC</em> genotype have greater reduction in SBP (mean difference –28.5 ± 15.2 for valsartan and vs. –32.3 ± 5.5 mmHg for amlodipine) in comparison with <em>CT</em> and <em>TT</em> genotypes, this difference did not reach the statistical significance (<em>P</em> value&gt; 0.05). Furthermore, the <em>CYP4F2 rs2108622</em> genotype was not associated significantly (<em>P</em> value&gt; 0.05) with valsartan and amlodipine responses after adjustment the responses with sex, BMI, age, and smoking status of the patients.</div></div><div><h3>Discussion</h3><div>While there is a trend suggesting <em>CYP4F2 rs2108622 CC</em> genotype may respond better to valsartan and amlodipine responses, the absence of statistical significance supports the need for larger pharmacogenetic studies.</div></div><div><h3>Conclusions</h3><div>It can be concluded from the findings of this study that there is a lack of association between the <em>CYP4F2 rs2108622</em> genotype and valsartan and amlodipine responses among a sample of Jordanians with essential hypertension.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"185 ","pages":"Article 107091"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148391641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond association: Mediation roles of lipidomics and cytokine in PCOS uncovered by cross-disciplinary genomics","authors":"Tingyu Lang,&nbsp;Yongxiu Yang","doi":"10.1016/j.prostaglandins.2026.107090","DOIUrl":"10.1016/j.prostaglandins.2026.107090","url":null,"abstract":"<div><h3>Background and aims</h3><div>Polycystic ovary syndrome (PCOS) is a metabolic disorder that significantly impacts female fertility. Lipids and inflammation are key factors in the pathogenesis and progression of PCOS. This study aims to elucidate the complex causal relationships involving 179 lipids, 91 inflammatory markers, and PCOS using robust Mendelian Randomization (MR) methods based on Genome-Wide Association Studies (GWAS). Additionally, we seek to quantify the mediating effects of inflammation markers on lipid in PCOS.</div></div><div><h3>Methods and results</h3><div>After rigorous screening of eligible SNPs, IVW was employed, supplemented by Simple mode, Weighted median, Weighted mode, and Bayesian Weighted Mendelian Randomization analyses. Sensitivity analyses were performed to ensure result accuracy. Mediation analysis was conducted to identify inflammation factors mediating the lipid-PCOS pathway. We identified 11 lipids causally associated with PCOS, including sterol esters, phosphatidylcholine, sphingomyelin, and triacylglycerol. MR Analysis linked these lipids to 58 inflammatory factors, of which only two were associated with PCOS, with β-NGF increasing the risk of PCOS by 6.50% and uPA reducing it by 4.60%. Mediator analysis showed the effect of uPA-mediated phosphatidylcholine (18:2_20:4) on PCOS.</div></div><div><h3>Conclusion</h3><div>This study is the first to use MR to explore causal links between lipids, inflammatory factors, and PCOS. We identified uPA as a key mediator and uncovered 11 lipids significantly associated with PCOS, highlighting the phosphatidylcholine (18:2_20:4)-uPA-PCOS pathway. Our findings suggest targeting lipid metabolism and using phosphatidylcholine (18:2_20:4) and uPA as biomarkers and tools for evaluating therapeutic efficacy in PCOS.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"185 ","pages":"Article 107090"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148309380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review on the mechanistics of free fatty acid-induced insulin resistance and it’s therapeutics: Molecular perspectives","authors":"Swati Banerjee,&nbsp;Subhajit Maity,&nbsp;Subhajit Ghosh,&nbsp;Arunodaya Gautam,&nbsp;Indrani Chakraborty,&nbsp;Nabin Baran Manik","doi":"10.1016/j.prostaglandins.2026.107092","DOIUrl":"10.1016/j.prostaglandins.2026.107092","url":null,"abstract":"<div><div>Type 2 diabetes mellitus (T2DM) is a multidimensional metabolic disorder characterized by hyperglycemia, insulin insensitivity, and dysfunction and degeneration of β-cells. Increase in the levels of free fatty acids (FFAs) in blood plasma is a typical symptom of obesity and metabolic syndrome, which influences the mechanisms of insulin resistance and β-cell impairment. Acute increase in FFA levels blocks glucose uptake by insulin-sensitive skeletal muscles while chronic increase in FFA levels results in hepatic insulin resistance which causes gluconeogenic flux and lipotoxicity in pancreatic βcells. FFA-induced insulin resistance involves various molecular pathways and generation of lipid intermediates (diacylglycerol and ceramides), activation of serine/threonine kinases (PKC), induction of oxidative and endoplasmic reticulum stresses, and inflammatory signaling via nuclear factor-κB (NF-κB) and toll-like receptor (TLR) signaling pathways. Recent studies have indicated that the fetuin-A-FFA complex is an important endogenous ligand of TLR4 that causes inflammation and metabolic dysregulation. In addition, certain FFAs, especially ω-6 polyunsaturated fatty acids, can elicit ferroptosis which is a new form of lipid peroxidation-mediated cell death in β-cells, thereby expanding the extent of FFA-mediated lipotoxicity. This review covers recent information on the mechanisms and clinical factors related to the role of FFAs in insulin resistance and T2DM pathogenesis, and the contribution of experimental research towards developing therapeutic strategies in normalizing the levels of FFA and inhibiting downstream lipotoxicity-related pathways.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"185 ","pages":"Article 107092"},"PeriodicalIF":2.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging induces the hepatic CYP4A–20-HETE axis with stage-dependent oxylipin remodeling","authors":"Lisha Wei ,&nbsp;Jian Hong ,&nbsp;Dehui Sun ,&nbsp;Qin Wu ,&nbsp;Yikai Huang ,&nbsp;Xiuke Ouyang ,&nbsp;Hualong Zhao ,&nbsp;Junyi Zheng ,&nbsp;Wenying Zhang ,&nbsp;Xuehong Tong ,&nbsp;Pei Wang ,&nbsp;Yu Bai ,&nbsp;Wei Qiu ,&nbsp;Yijun Kang ,&nbsp;Xuena Zhang","doi":"10.1016/j.prostaglandins.2026.107080","DOIUrl":"10.1016/j.prostaglandins.2026.107080","url":null,"abstract":"<div><div>Hepatic inflammaging is a prominent feature of aging, yet the timing and pathway architecture of hepatic oxylipin remodeling remain unclear. Here, we integrated liver histopathology with targeted LC–MS/MS profiling of oxylipins across 2, 12, 18, and 24 months in male Sprague–Dawley rats, and related mediator shifts to age-associated regulation of key metabolic enzymes, supported by human patterns. Aging was accompanied by progressive inflammatory infiltration and steatotic remodeling, alongside clear separation of hepatic oxylipin landscapes. By midlife (12–18 months), ω-6 outputs were enriched for arachidonic acid (AA)–linked mediators, including 8-iso-PGF₂α, tetranor-12(S)-HETE, and the CYP4A-associated ω-hydroxylation product 20-HETE, whereas selected linoleic acid (LA) epoxide/diol derivatives declined. In late aging (24 months), hepatic resolvin E1 (RvE1) decreased markedly despite preserved or increased ω-3 substrates/intermediates, coinciding with accumulation of DHA-derived oxidation products. These changes paralleled induction of <em>Cyp4a8</em> and suppression of <em>Alox15</em>, and human data revealed partially aligned age-associated patterns in selected pathway-related markers in hepatic <em>CYP4A11</em>/<em>ALOX15</em> expression and circulating mediators. Collectively, we define a staged hepatic oxylipin imbalance during aging, characterized by heightened CYP4A/20-HETE tone and attenuated ALOX15/RvE1-associated resolution.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"184 ","pages":"Article 107080"},"PeriodicalIF":2.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148056444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Pharmacological modulation of NF-κB–dependent COX-2/PGE₂ signaling influences inflammatory lesion development during Leishmania mexicana infection” [Prostaglandins Other Lipid Mediat. 184 (2026) 107075]","authors":"Verónica I. Hernández Ramírez,&nbsp;Carlos Osorio-Trujillo,&nbsp;E. Gisela Martínez-Romero,&nbsp;José A. Diaz-Gandarilla,&nbsp;Raúl Argüello-García,&nbsp;Lidia Baylon-Pacheco,&nbsp;Luis A. Constantino-Jonapa,&nbsp;María Maylen Arrieta-González,&nbsp;Daniela Eloísa San Juan-Mora,&nbsp;Patricia Talamás-Rohana","doi":"10.1016/j.prostaglandins.2026.107078","DOIUrl":"10.1016/j.prostaglandins.2026.107078","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"184 ","pages":"Article 107078"},"PeriodicalIF":2.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of COX–2 inhibition by DuP–697 on cyclin B1/Cdc2 dynamics in human medullary thyroid carcinoma cells","authors":"Chien-Chen Lu Ph. D.","doi":"10.1016/j.prostaglandins.2026.107079","DOIUrl":"10.1016/j.prostaglandins.2026.107079","url":null,"abstract":"<div><h3>Background</h3><div>Cyclooxygenase–2 (COX–2) and its product prostaglandin E₂ (PGE₂) are key mediators of parafollicular cell proliferation and calcitonin secretion in medullary thyroid carcinoma (MTC). Although COX–2 inhibitors exhibit anti–proliferative effects, the molecular mechanisms underlying their influence on cell–cycle regulation remain unclear.</div></div><div><h3>Objective</h3><div>This study explored the effects of the selective COX–2 inhibitor DuP–697 on proteins associated with G₂/M regulatory signaling in human medullary thyroid carcinoma TT cells.</div></div><div><h3>Methods</h3><div>TT cells were treated with DuP–697 (40–160 nM) for 3–72 h. Immunofluorescence analyses were performed to quantify cyclin B1, phosphorylated Cdc2 (Tyr15), Myt1, phosphorylated Wee1, p21, and phosphorylated histone H3.</div></div><div><h3>Results</h3><div>DuP–697 induced time–dependent alterations in multiple proteins associated with G₂/M regulation. Early exposure (3–24 h) was associated with increased cyclin B1 and phosphorylated Cdc2, accompanied by transient elevation of phosphorylated histone H3. With prolonged treatment (48–72 h), phosphorylated histone H3 levels declined, while Myt1 expression remained persistently elevated and phosphorylation of Wee1 displayed dynamic modulation. In parallel, p21 expression was selectively reduced at intermediate and late time points. These coordinated changes suggest a shift in the balance of G₂/M–associated regulatory signals over time.</div></div><div><h3>Conclusion</h3><div>Taken together, these findings indicate that DuP–697 is associated with time–dependent modulation of proteins involved in G₂/M regulatory signaling in TT cells. Rather than providing direct evidence of cell–cycle arrest, the results support an exploratory model in which COX–2 inhibitor exposure is accompanied by dynamic reorganization of mitotic and checkpoint–related regulatory components. Further functional studies, including direct assessment of cell–cycle distribution and mitotic progression, are required to clarify the biological consequences of these regulatory changes.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"184 ","pages":"Article 107079"},"PeriodicalIF":2.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148056508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}