Molecular and Cellular Biochemistry最新文献

{"title":"Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.","authors":"Faezeh Sharafi, Elham Rismani, Mohamad Rhmanian, Arezoo Khosravi, Ali Zarrabi, Massoud Vosough","doi":"10.1007/s11010-025-05377-x","DOIUrl":"10.1007/s11010-025-05377-x","url":null,"abstract":"<p><p>Globally, liver cancer is reported to be the third leading cause of cancer-related mortality. The most common type of these cancers is hepatocellular carcinoma (HCC). Current preventive strategies, including lifestyle modifications, antiviral therapies, and surveillance, are limited in their effectiveness. Mitochondria play critical roles in regulating cellular metabolism, oxidative stress, and apoptosis. Mitochondrial dysfunction can accelerate HCC progression, particularly in patients with liver diseases such as metabolic-associated fatty liver disease (MAFLD) and metabolic dysfunction-associated steatohepatitis (MASH). In this review, we discuss the mechanisms of mitochondrial dysfunction in HCC from a molecular point of view, including oxidative stress, mitophagy dysregulation, mitochondrial dynamics dysregulation, and mitochondrial DNA (mtDNA)-mediated dysregulation of innate immune responses. Additionally, we explore molecular-targeted therapies aimed at restoring mitochondrial function. Critical approaches include targeting reactive oxygen species pathways through agents such as iridium (III) complexes and Mito Rh S, which induce cancer cell death through apoptosis and ferroptosis. Other compounds, including dehydrocrenatidine, enhance oxidative phosphorylation and promote apoptosis. Inhibitors of dynamin-related protein 1 (Drp1) target mitochondrial fission to reduce tumor growth. Furthermore, mitophagy modulators, such as SIRT1 activators, improve mitochondrial quality control, minimize the negative effects of oxidative stress, and reduce cancer development. Clinical trials are ongoing for the mitochondrial enzyme-targeting agents CPI-613 and Gamitrinib, a heat shock protein-targeting agent, which have hence shown great promise for these therapies. With further investigation, mitochondrial-targeted interventions could be promising for preventing or reducing HCC incidence and recurrence, increasing long-term survival, and improving the quality of life of patients with advanced-stage disease.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Administration of a recombinant secretory leukocyte protease inhibitor prevents aortic aneurysm growth in mice.","authors":"Aika Yamawaki-Ogata, Masato Mutsuga, Yuji Narita","doi":"10.1007/s11010-025-05374-0","DOIUrl":"https://doi.org/10.1007/s11010-025-05374-0","url":null,"abstract":"<p><p>Pharmacological interventions to inhibit the progression of aortic aneurysm (AA) have not yet been established. We previously reported that mesenchymal stem cells (MSCs) provide a potential foundation for less invasive treatment of AA. In this study, we investigated the secretory proteins from MSC supernatants to clarify the therapeutic effects of MSCs. Furthermore, we treated thoracoabdominal aortic aneurysm (TAAA) mice with two anti-inflammatory proteins from among these secretory proteins to confirm their therapeutic effects. Protein profiles of MSC-secreted factors were analyzed using protein microarrays, and two anti-inflammatory proteins, namely progranulin (PGRN) and secretory leukocyte protease inhibitor (SLPI), were identified. Apolipoprotein E-deficient mice were continuously infused with angiotensin II via an osmotic pump for 4 weeks to induce TAAA formation, and then recombinant rPGRN and/or rSLPI were administered intraperitoneally. Mice were sacrificed at 8 weeks, and aortas were analyzed for protein expression and also stained with Elastica van Gieson and immunofluorescence to detect inflammatory cells. Intraperitoneal administration of rSLPI inhibited TAAA growth more than rPGRN alone or the combination of rPGRN and rSLPI, by inducing the following effects: downregulation of inflammatory cytokines and chemokines, specifically IL-1β, IL-6, TNF-α, and MCP-1; reduced NO production; decreased phosphorylated NF-κB levels; and decreased elastin destruction and infiltration of inflammatory cells. We identified anti-inflammatory proteins, including PGRN and SLPI, in the MSC supernatants and showed that the administration of rSLPI inhibited TAAA progression in mice. These promising preliminary data present a new approach for the treatment of less invasive TAAA.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic stress, gut microbiota, and immunity: interconnections and implications for health.","authors":"Hexiao Jia, Xiaodong Guo, Yihong Wei, Can Can, Na He, Hailei Zhang, Xinyu Yang, Hanyang Wu, Wancheng Liu, Daoxin Ma","doi":"10.1007/s11010-025-05376-y","DOIUrl":"https://doi.org/10.1007/s11010-025-05376-y","url":null,"abstract":"<p><p>Psychological stress influences the hypothalamic-pituitary-adrenal (HPA) and the sympathetic-adrenal -medullary (SAM) axes which directly impact the immune system. Stress not only affects hematopoietic stem cell activity but also increases the circulating levels of inflammatory cells, thereby potentially exacerbating pathogenic conditions. Moreover, stress affects hormone release, inflammation, and autonomic changes, which can modify the composition of the gut microbiota and indirectly alter the immune system. This review aims to summarize the research that demonstrates the relationships among stress, the gut microbiota, and hematopoiesis to increase our understanding of the intricate connections among them, while also highlighting the bidirectional influences among chronic diseases, systemic inflammation, and stress.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NETs accelerate aortic valve calcification by promoting M1 macrophage polarization through the TLR9 signaling pathway.","authors":"Luyao Liu, Zhenzhen Lan, Xincan Liu, Yun Chen, Zhihao Chen, Li Cheng, Ting Hu","doi":"10.1007/s11010-025-05375-z","DOIUrl":"https://doi.org/10.1007/s11010-025-05375-z","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs) are positively correlated with the severity of calcific aortic valve disease (CAVD). This study aims to elucidate the mechanism by which NETs contribute to CAVD. The CAVD mice model was established by calcification-promoting diets, and NETs formation was modulated via intraperitoneal injection of Cl-amidine. We observed the effect of NETs on Raw264.7 cells by regulating NETs and TLR9 in vitro. Concentrations of TNF-α, MPO-DNA complex, and IL-10 were measured using ELISA. NETs formation was assessed through immunofluorescence assay citrullinated histone H3 (citH3). Expression levels of BMP2, RUNX2, IL-1β, TNF-α, IL-10, and TLR 9 were analyzed by qRT-PCR and Western blotting, while flow cytometry was used to assess the expression of CD86 and CD206 on Raw264.7 cells. Results indicated that compared to the vehicle group, the CAVD group exhibited significant valve thickening and increased calcium deposition, as well as elevated levels of inflammatory factors TNF-α and IL-1β, NET-related markers MPO-DNA complexes and citH3, ossification factors BMP2 and RUNX2, and TLR9. Conversely, IL-10 levels were significantly reduced. Cl-amidine intervention in early CAVD mice significantly improved valve thickness and reduced calcium deposition, inflammatory factors, NETs-related markers, ossification factors, and TLR9 levels, while increasing IL-10 levels. Cl-amidine may delay CAVD progression in mice by reducing NETs. In vitro studies confirmed that serum from CAVD mice induced NETs, promoting the polarization of Raw264.7 cells to the M1 phenotype via TLR9 signaling pathway, thereby releasing pro-inflammatory factors (TNF-α, IL-1β, and IL-6), and inhibiting M2 polarization and IL-10 expression. In summary, our findings suggest that NETs promote Raw264.7 cell polarization to M1 through the TLR9 signaling pathway, contributing to the inflammatory response in CAVD. This study proposes a novel therapeutic strategy targeting NETs to delay CAVD progression.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermittent fasting and exercise: a dual intervention for orchestrating glycolipid conversion and utilization in healthy mice.","authors":"Xueping Wu, Jian Shi, Junming Wang, Weiye Li, Jingxin Chen, Ruiying Lyu, Chunhong Liu","doi":"10.1007/s11010-025-05372-2","DOIUrl":"https://doi.org/10.1007/s11010-025-05372-2","url":null,"abstract":"<p><p>Intermittent fasting (IF) and exercise can reverse the impaired glycolipid conversion ability caused by obesity. However, the effects of IF and exercise combination on glycolipid conversion ability in normal individuals remain to be determined. In this study, male KM mice were subjected to IF (including alternate-day fasting (ADF), time-restricted fasting (TRF)), treadmill exercise, and a combination of the two interventions for 6 weeks. The effects of two IF models combined exercise on glycolipid conversion in mice were investigated by detecting serum biochemical indexes, and the expressions of genes and proteins closely related to the glycolipid conversion pathway in liver, gastrocnemius, and inguinal adipose tissue. The results showed that IF combined with exercise significantly reduced fasting blood glucose, glycated serum protein and liver glycogen levels in mice. TRF combined with exercise significantly decreased triglyceride levels in serum, liver and gastrocnemius. IF combined with exercise activated the ChREBP or SREBP1/FASN pathways to enhance the transcriptional activation of the glucose-mediated adipogenesis pathway, and simultaneously promoted the expression of fatty acid oxidation proteins and reduced liver gluconeogenesis genes expression, collectively improving lipid metabolic efficiency. Furthermore, IF increased the expression of glycogen turnover-related protein PPP1R3C and adipose thermogenesis-related protein UCP1 in the inguinal adipose tissue, indicating enhanced glycogen flux coordination with adipose thermogenic activation. In conclusion, IF combined with exercise orchestrates the glycolipid conversion and substrate utilization.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of intestinal microbiota in patients with psoriasis combined with metabolic syndrome.","authors":"Yiyue Yuan, Linna Zhao, Haining Ding, Yinshuang Hua, Hongmei Wang, Manlin Zhao","doi":"10.1007/s11010-025-05370-4","DOIUrl":"https://doi.org/10.1007/s11010-025-05370-4","url":null,"abstract":"<p><p>The co-morbidity of psoriasis (PsO) and metabolic syndrome (MetS) is prevalent. While the mechanisms causing PsO in MetS remain unknown, it is understood that gut microbiota plays a critical role in maintaining immune and metabolic balance. However, the specific mechanisms and whether biomarkers are involved in the pathophysiological process of PSO in MetS patients have yet to be elucidated. This study involved 29 patients with PSO and MetS (PM) and 29 with MetS (M). It analyzed their clinical parameters, microbial composition, function, diagnostic, and predictive performance. The results unveiled significant differences between the two groups concerning microbial diversity and community composition. Most of the differential microbiota in the PM group exhibited a negative correlation with high-density lipoprotein (HDL) and a positive correlation with serum uric acid (SUA). In contrast, the opposite was observed in the M group. Sixteen MetaCyc pathways showed significance in the PM group, encompassing peptidoglycan biosynthesis II (staphylococci), the super pathway of L-arginine and L-ornithine degradation, teichoic acid (poly-glycerol) biosynthesis, and palmitic biosynthesis II (bacteria and plants). Six KEGG pathways were enriched in the M group, such as flavone, flavonol biosynthesis, and carotenoid biosynthesis. Most importantly, we determined that eight biomarkers, represented by Akkermansia, demonstrated robust diagnostic predictive power. This study elucidates the potential mechanism through which metabolic disorders impact the onset and progression of psoriasis via intestinal microbiota. Furthermore, it offers novel strategies for preventing, diagnosing, and treating PsO in MetS.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal effect of systolic blood pressure on myocardial injury and mortality: insights from Mendelian randomization and a prospective group study.","authors":"Chuting Wang, Huadong Tang, Qiuxiang Yang, Yagui Lu, Zhijian Lin, Yuekui Zhang","doi":"10.1007/s11010-025-05373-1","DOIUrl":"https://doi.org/10.1007/s11010-025-05373-1","url":null,"abstract":"<p><p>This study aimed to examine the causal relationship between systolic blood pressure (SBP) and myocardial injury (MI), and to evaluate its prognostic implications for all-cause and cardiovascular mortality. A two-stage analytical approach was used. First, Mendelian randomization (MR) was conducted to assess the independent causal effects of SBP on six MI-related phenotypes, with adjustment for potential confounders, including lipid profiles, glycemic indices, and anthropometric traits. Second, data from 4459 participants in the National Health and Nutrition Examination Survey, with a follow-up period of up to 15 years, were analyzed. The dose-response relationship between SBP and MI was assessed using restricted cubic spline analysis. Thresholds based on sex-, age-, and comorbidities were identified using the Johnson-Neyman interaction model. MR analysis demonstrated a causal association between elevated SBP and increased risks of acute heart failure (odds ratio [OR] = 1.523), MI (OR = 1.014), and ischemic stroke (OR = 33.339). In the prospective group analysis, SBP ≥ 180 mmHg was associated with a 213.4% increased risk of MI (OR = 3.134, p = 0.003), and a graded increase in mortality was observed (hazard ratio [HR] = 2.783 for all-cause death; HR = 1.888 for cardiovascular death). Sex-stratified analysis demonstrated that the lowest MI risk occurred at SBP levels of 120-150 mmHg in men and extended to 162 mmHg in women. Among individuals aged ≥ 43 years, the risk of all-cause mortality significantly increased when SBP exceeded 135 mmHg (p < 0.001). A U-shaped relationship between SBP and mortality was observed in individuals aged ≥ 58 years with MI, with the lowest risk at 113 mmHg. Genetic and observational evidence support a causal role of elevated SBP in the development of MI. The findings demonstrate sex- and age-specific thresholds, along with a U-shaped mortality curve, providing a nuanced framework for individualized blood pressure management strategies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of exosomes derived from platelet-rich plasma during human sperm cryopreservation.","authors":"Fatemeh Karimi, Marzieh Kafami, Fatemeh Ghodrati Khakestar, Mohammad Hossein Madahali, Samad Nazemi, Sareh Karimi","doi":"10.1007/s11010-025-05371-3","DOIUrl":"10.1007/s11010-025-05371-3","url":null,"abstract":"<p><p>Fertility preservation is a critical aspect of improving human life quality. Sperm cryopreservation is highly recommended for men at risk of infertility; however, it can have detrimental effects on sperm quality. In this study, we evaluate the effects of platelet-rich plasma (PRP) and PRP-derived exosomes on cryopreservation outcomes in men with asthenoteratozoospermia referred to a public infertility center. The semen samples from 75 men with asthenoteratozoospermia (based on WHO 2020 criteria) were randomly divided into five groups: Control (conventional freezing), Exo/before, Exo/After, PRP/Before, and PRP/After. In all intervention groups, PRP or exosomes were added either 1 h before freezing or 1 h after thawing. Sperm parameters and oxidative stress were evaluated in all samples. Sperm incubation with exosomes before freezing significantly improves motility and lowers DNA fragmentation index (DFI) and oxidative stress compared to the control and other groups. Based on the present study, semen incubation with exosomes for 1 h before freezing not only protects sperm against oxidative stress but also enhances some sperm parameters, such as motility, in men with asthenoteratozoospermia.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the enigma: long noncoding RNAs in disease pathogenesis and therapeutic prospects.","authors":"Palaniappan Ramesh, Pallavi Muthyala, Suresh Kumar Kali","doi":"10.1007/s11010-025-05368-y","DOIUrl":"https://doi.org/10.1007/s11010-025-05368-y","url":null,"abstract":"<p><p>Despite advancements in disease understanding and therapeutic interventions, the global burden of diseases continues to increase rapidly, emphasizing the need for novel insights and approaches. Long noncoding RNAs (lncRNAs) have emerged as key players in biological processes and influence gene expression regulation and cellular signalling pathways. This review explores the complex roles of lncRNAs in modulating chromatin function, regulating nuclear bodies, and impacting posttranslational modifications. Moreover, their interactions with various RNA species and proteins significantly influence cell signalling cascades, thereby contributing to diverse pathophysiological conditions, including cancer, neurological disorders, metabolic syndromes, and autoimmune diseases. We highlight the potential of lncRNAs as diagnostic biomarkers and therapeutic targets in clinical settings. By describing the complex involvement of lncRNAs in disease mechanisms, this review aims to stimulate further research in this field, encouraging a deeper understanding of disease pathogenesis and paving the way for innovative therapeutic strategies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HuD and alpha-crystallin A axis protects neuro-retinal cells in early diabetes.","authors":"Chongtae Kim, Subeen Oh, Young-Hoon Park","doi":"10.1007/s11010-025-05364-2","DOIUrl":"https://doi.org/10.1007/s11010-025-05364-2","url":null,"abstract":"<p><p>Diabetic retinopathy (DR) is a prevalent microvascular complication of diabetes; however, neuro-retinal degeneration is also observed in patients with diabetes without signs of DR. The mechanisms leading to neuro-retinal cell loss before vascular complications manifest in diabetes remain poorly understood. In this study, we investigated the neuronal RNA-binding protein HuD as a novel regulator of neuro-retinal degeneration in the early stage of diabetes. We determined the expression of HuD and alpha-crystallin A (CRYAA) in the retinal ganglion cell layer. HuD and CRYAA were down-regulated in the retinas of streptozotocin-induced diabetic rats and in neuro-retinal cells (R-28) treated with high glucose. Cryaa mRNA was identified as a novel target transcript of HuD, and we demonstrated that HuD post-transcriptionally regulates the expression of Cryaa mRNA by binding to its 3'-untranslated region. Silencing and overexpression of HuD positively regulated the expressions of Cryaa mRNA and protein. We demonstrated that the increase in inflammatory cytokines such as TNFα, IL-1β, and IL-6 in R-28 cells under hyperglycemic conditions was a result of both CRYAA and HuD levels. Silencing HuD and CRYAA enhanced high glucose-induced R-28 cell death, whereas their overexpression alleviated this effect. HuD post-transcriptionally regulates CRYAA expression, influencing the function and viability of neuro-retinal cells under diabetic conditions. Our results suggest that the HuD/CRYAA axis plays a crucial role in neuro-retinal cells and has the potential to serve as a prognostic factor and therapeutic target for diabetic neuro-retinal degeneration.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}