Journal of physiology and biochemistry最新文献

{"title":"Decoding dysbiosis: the role of gut microbiota in MASLD progression and emerging therapeutic interventions.","authors":"Dinesh Mohan Swamikkannu, Santhosha Dasarapu, Kanishk Dinesh Mohan, Allimalarkodi Shanmugam","doi":"10.1007/s13105-026-01199-7","DOIUrl":"https://doi.org/10.1007/s13105-026-01199-7","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), affects a substantial proportion of the global population and is closely associated with metabolic disorders. The gut microbiota, comprising a diverse community of microorganisms within the gastrointestinal tract, plays a crucial role in maintaining host health. Dysbiosis, defined as an imbalance in this microbial ecosystem, has been increasingly implicated in the development and progression of liver diseases, including MASLD. This review examines the role of the gut microbiota in MASLD pathogenesis and highlights its potential as a therapeutic target. The gut-liver axis facilitates bidirectional communication between the intestine and the liver, thereby influencing metabolic regulation. In MASLD, dysbiosis characterized by reduced microbial diversity and an increased abundance of Gram-negative bacteria leads to altered bile acid metabolism, increased intestinal permeability, enhanced endotoxin translocation, and hepatic inflammation. Additionally, it disrupts short-chain fatty acid production and interferes with the endocannabinoid system and choline metabolism, collectively driving disease progression. Emerging non-invasive diagnostic approaches, including gut microbiome profiling, show promise for early detection. Although specific pharmacological treatments remain limited, microbiota-targeted strategies such as probiotics, prebiotics, and synbiotics aim to restore microbial balance. Furthermore, emerging modalities within microbiome-based therapies, including mesenchymal stromal cell therapy and bacteriophage therapy, offer potential for targeted modulation of the gut microbiota and liver repair. The gut microbiota-liver axis plays a central role in the pathogenesis of MASLD. Growing insights into this relationship have driven the development of microbiome-based diagnostic and therapeutic approaches. Non-invasive diagnostic tools, particularly gut microbiome profiling, show promise for early detection. Therapeutically, microbiota-targeted strategies including probiotics, prebiotics, synbiotics, and emerging modalities such as cellular and bacteriophage-based therapies offer potential to restore microbial balance and improve liver function. Nevertheless, robust clinical studies are essential to validate their efficacy, safety, and applicability in personalized MASLD management.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897439","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":"Potassium channels in cancer: from hallmarks to therapeutic targeting.","authors":"Yi-Ling Zhang, Rong-Jia Shi, Xin-Hua Liang","doi":"10.1007/s13105-026-01228-5","DOIUrl":"https://doi.org/10.1007/s13105-026-01228-5","url":null,"abstract":"<p><p>Potassium channels constitute important signaling nodes in the progression of human cancers. Through canonical ion conduction-dependent functions, including intracellular K⁺ homeostasis, membrane potential and associated Ca²⁺ signaling, and cell volume, they influence proliferation, cell death, phenotypic plasticity, invasion and metastasis, metabolic reprogramming, and angiogenesis. Beyond ion conduction, potassium channels may affect malignant phenotypes through non-canonical mechanisms, including conformational signaling, protein interactions, transcriptional regulation, and auxiliary-subunit functions. They also contribute to tumor microenvironment remodeling by regulating immune and stromal cells and altering antitumor immune responses. However, their biological effects vary with channel subtype, tumor type, functional state, and non-canonical protein interactions, resulting in oncogenic or tumor-suppressive activity. This heterogeneity makes it hard to infer channel function from expression levels alone and also limits the development of selective therapeutic strategies. This review integrates evidence on the canonical and non-canonical functions of potassium channels across distinct cellular contexts, explains the mechanistic basis of their opposing effects, and evaluates their therapeutic potential and the major challenges to clinical translation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873062","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":"Exercise elicits mitonuclear protein imbalance and UPR^mt in the liver of mice with obesity.","authors":"Matheus Biscaro Rocha, Izabela Monteiro de Araujo, Saulo Gabriel do Nascimento Della Coleta, Scylas J A Junior, Sidney F Peres, Renata R Braga, Rafael S Brícola, Fernanda S Carneiro, Barbara M Crisol, Raul G da Costa, Marcelo A S Mori, Dennys E Cintra, Adelino S R da Silva, José R Pauli, Eduardo Rochete Ropelle","doi":"10.1007/s13105-026-01229-4","DOIUrl":"10.1007/s13105-026-01229-4","url":null,"abstract":"<p><p>Mitochondrial dysfunction plays a critical role in the development of metabolic dysfunction-associated steatotic liver disease (MASLD). It has been proposed that mitochondrial unfolded-protein response (UPR^mt) activation improves mitochondrial function in the liver. Growing evidence demonstrates that physical exercise effectively prevents and treats MASLD. However, the effects of exercise on UPR^mt activation in the liver are unknown. Thus, we investigated the impact of aerobic training on the mechanisms involved in mitochondrial quality control in the liver in a mouse model of obesity. Liver transcript data from a genetic reference panel of BXD isogenic mice revealed a negative correlation between UPR^mt-related genes and hepatic triacylglycerol content. In addition, the liver UPR^mt markers were strongly associated with several mitochondrial-related genes in the hepatic tissue of BXD mice and humans. Notably, 4 weeks of aerobic exercise strongly impacted the liver metabolism, preventing intrahepatic lipid accumulation in HFD-fed mice. Physical exercise boosted the NAD-biosynthesis pathway, elicited the mitonuclear protein imbalance, stimulated the protein content of UPR^mt-markers, including CLpP, Lonp1, and Yme1L1, and improved the mitochondrial proteostasis and function in the liver in HFD-fed mice. Thus, our findings link the mitonuclear protein imbalance and UPR^mt activation in the liver to mitochondrial proteostasis and MASLD prevention in response to physical exercise.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874502","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":"Correction: Unveiling the role of CB2 receptor in beta-hydroxybutyrate mediated modulation of microglial anti-inflammatory phenotype.","authors":"Monika Iešmantaitė, Liutauras Usonis, Kristupas Čeika, Egidijus Šimoliūnas, Mantas Liudvinaitis, Nerea Soto-Arroyo, Isabel Moreno-Indias, Francisco J Tinahones, Daiva Baltriukienė, Virginia Mela","doi":"10.1007/s13105-026-01222-x","DOIUrl":"10.1007/s13105-026-01222-x","url":null,"abstract":"","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148850878","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":"Early-life overconsumption of a high-carbohydrate diet induces metaflammation and kidney injury without impairment of function in adult Wistar rats.","authors":"Cristhian Neftaly Sánchez-Solís, Hugo Hernández-Fragoso, Alfonso Diaz, Rubén Vázquez-Roque, Olivier Christophe Barbier, José Everardo Avelino-Cruz, Samuel Treviño","doi":"10.1007/s13105-026-01226-7","DOIUrl":"10.1007/s13105-026-01226-7","url":null,"abstract":"<p><p>Frequent consumption of sugary and calorie-dense foods and beverages during childhood may contribute to the development of metabolic syndrome (MetS) in adulthood, a risk that can manifest independently of overweight status. Metaflammation, a low-grade inflammation associated with MetS, can induce functional loss in multiple tissues, including the kidneys, potentially signaling the onset of damage. This work aimed to evaluate the progressive structural changes, damage, and kidney function associated with metaflammation-induced MetS in young to adult Wistar rats. Early-life rats were divided into two groups: one fed a standard diet and the other a high-carbohydrate diet (HCD). Three analysis time points were designed: 6 weeks (adolescence), 12 weeks (young adulthood), and 20 weeks (adults). Zoometry, nutritional status, metabolic biomarkers, kidney function, serum and urinary cytokines, and kidney injury molecule 1 (KIM-1) were measured in each cohort. Histopathologic modifications, inflammation, and redox balance were analyzed in the renal cortex. Results show that HCD consumption progressively induces MetS and metaflammation, increasing serum levels of inflammatory cytokines and KIM-1. However, renal function was not affected. Renal cortex inflammation began in adolescence, even before oxidative stress was established in young and adult rats. The renal tissue showed hallmarks of early kidney damage, including mesangial cell expansion, podocyte loss, hypertrophy, tubular hyperplasia, and fibrosis. In urine, levels of KIM-1, TGF-β, and IL-1β increased. In conclusion, chronic HCD consumption from early life establishes MetS and metaflammation, leading to silent nephropathy. This state is characterized by structural remodeling and profibrotic signaling that occur independently of standard clinical kidney function markers in Wistar rats.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13503461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148813403","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":"Unveiling the role of age in MASLD development and biological process activation: Implications for translational research.","authors":"Lucía Lameroli Mauriz, Andrea Scelza-Figueredo, Miranda Sol Orellano, Brian L Martínez Ruiz, Juan Bayo, Esteban Fiore, María José Cantero, Barbara Bueloni, Mailin Casadei, Maite G Fernandez-Barrena, Matias A Avila, Luz Andreone, Guillermo D Mazzolini, Catalina Atorrasagasti","doi":"10.1007/s13105-026-01217-8","DOIUrl":"https://doi.org/10.1007/s13105-026-01217-8","url":null,"abstract":"<p><p>Age is a risk factor for severity and progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), yet its specific contributions to liver injury and molecular alterations remain unclear. Current animal models often overlook this variable. This study investigates how aging influences MASLD progression in a murine model, focusing on histological, biochemical, and transcriptomic differences. Young (2-month-old) and middle-aged (10-month-old) C57BL/6N male and female mice were fed chow (CD) or high-fat diet (HFD) for 20 weeks. Metabolic and biochemical parameters were assessed, and liver tissue analyzed by histology and RNA sequencing. Differentially expressed genes were identified with Limma, followed by gene ontolgy enrichment. Translational relevance was evaluated using the MASLD Human Proximity Score (MHPS). Middle-aged males developed insulin resistance and more severe hepatic injury than young males after HFD. Histological and biochemical assessments confirmed advanced disease in middle-aged mice, with extensive lipid accumulation, hepatocellular hypertrophy, inflammation and fibrosis. Females showed milder damage. Diet was the main determinant of transcriptomic changes in males: young HFD mice activated tissue remodeling pathways, whereas middle-aged mice showed inflammatory activation and reduced energy metabolism. In females, transcriptomic responses were attenuated, with metabolic and stress-related changes restricted mostly to young HFD animals. MHPS ranked the middle-aged male model highest in similarity to human MASLD. Age is a critical determinant of hepatic responses to dietary stress, with sex-specific modulation. The middle-aged male model closely mirrors human MASLD, providing a more relevant preclinical platform to improve patient stratification and therapeutic discovery.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794796","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":"The endocannabinoidome-microbiota axis in obesity: a potential link to colorectal cancer development.","authors":"Gabriela Ávila Alpino, Poliana Guiomar Brasiel, Mariana M Almeida, Sheila C P Dutra Luquetti","doi":"10.1007/s13105-026-01225-8","DOIUrl":"10.1007/s13105-026-01225-8","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a multifactorial disease strongly influenced by genetic and environmental factors, as well as by immune and metabolic disorders such as obesity and gut dysbiosis. Recent evidence highlights the interplay between the endocannabinoidome (eCBome) and the gut microbiota as a central regulatory axis of intestinal homeostasis, metabolism, and immune responses. Although no studies have directly investigated this functional interaction in the CRC context, recent evidence suggests that dysfunction of the eCBome-microbiota axis, commonly observed in obesity, may influence colorectal tumorigenesis by impairing intestinal barrier integrity, increasing endotoxemia and immune dysregulation, altering microbial metabolite production, and activating NF-κB-mediated pro-tumorigenic signaling pathway. This is the first review to comprehensively integrate current evidence linking obesity-associated eCBome-microbiota dysfunction with CRC-related mechanisms and to propose potential pathways through which this interaction may influence CRC pathogenesis, providing a framework to guide future studies and support the development of novel preventive and therapeutic strategies for CRC.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13498644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794752","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":"Label-free proteomic profiling identifies ECM-related alterations across regeneration states in human peripheral axonal neuropathies.","authors":"Marina Damato, Soulaimane Aboulouard, Velia La Pesa, Francesco Gentile, Giulia Lunghi, Michela Perrone, Beatrice Pranzo, Elena Chiricozzi, Nilo Riva, Isabelle Fournier, Alessandro Romano, Angelo Quattrini, Michel Salzet, Michele Maffia","doi":"10.1007/s13105-026-01219-6","DOIUrl":"https://doi.org/10.1007/s13105-026-01219-6","url":null,"abstract":"<p><p>Understanding the multiple mechanisms underlying peripheral nerve regeneration in humans is crucial for developing effective therapies for peripheral axonal neuropathies. Although in vitro and in vivo studies have provided significant insights, human studies exploring the composition of proteome remain limited. The ECM plays a crucial role in nerve regeneration, influencing cell adhesion, proliferation, migration, and finally differentiation. In this study, we used a high-sensitivity, label-free liquid chromatography-mass spectrometry (LC-MS) method to investigate the global proteomic profile of human sural nerves aiming to identify molecular dynamics that promote or hinder nerve regeneration in well-characterized cohorts of patients with acute axonal injury, regenerating axonal neuropathy, and non-regenerating axonal neuropathy. Overall, 149 proteins were identified, of which 68 showed significant modulation across the groups. Proteins over-represented in regenerating nerves highlighted the multifactorial nature of regeneration, including immune modulation, debris clearance, cytoskeletal reorganization, axonal extension, and lipid transport. Conversely, structural myelin and neuronal proteins were significantly downregulated in non-regenerating nerves. Among the differentially expressed proteins, functional enrichment analysis revealed a significant overrepresentation of ECM-related components, providing compelling evidence that the ECM is not merely a passive scaffold, but an active driver of peripheral nerve regeneration.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13490253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794705","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":"Astrocytes orchestrate neuroprotection and pathogenesis via bidirectional neuronal interactions in Parkinson's disease.","authors":"Yifan Li, Qiang Li, Yemin Wang, Xuejing Wang, Guangfu Di, Meng Niu, Zhiliang Xu, Yanjiao Huang","doi":"10.1007/s13105-026-01218-7","DOIUrl":"https://doi.org/10.1007/s13105-026-01218-7","url":null,"abstract":"<p><p>Parkinson's disease (PD), a prevalent neurodegenerative disorder, is characterized by the degeneration of dopaminergic neurons in the substantia nigra and striatum of the midbrain, manifesting as distinct motor impairments. While conventional theories attribute PD's development to neuronal damage, astrocytes have garnered significant attention for their potential protective role. As the most abundant glial cells in the central nervous system (CNS), astrocytes may exert neuroprotective effects through mechanisms including secretion of neurotrophic factors, regulation of the blood-brain barrier (BBB), and maintenance of water-electrolyte balance. Recent studies indicate that mutations in PD-associated genes may induce functional alterations in astrocytes. Activated astrocytes accelerate neuronal degeneration by releasing inflammatory mediators, disrupting glutamate homeostasis, and triggering oxidative stress. Furthermore, bidirectional regulatory interactions exist between astrocytes and both dopaminergic neurons and other glial cells in PD. This review systematically summarizes current research on astrocyte involvement in PD pathology and their neuronal interaction mechanisms, further exploring their interconnections to elucidate disease pathogenesis. The findings provide novel theoretical frameworks for developing astrocyte-targeted therapies and preventive strategies against PD.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759682","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":"The LKB1-AMPK pathway in NAFLD: molecular mechanisms and therapeutic implications.","authors":"Pouya Goleij, Mohammad Amin Khazeei Tabari, Yousef Naser, Rayan Alataa, Mohammed Ali Mohammed Osman, Aryan Rezaee, Michael Aschner, Ahmed Rabie Dahab Ahmed, Moaad Abou Safrah, Haroon Khan","doi":"10.1007/s13105-026-01215-w","DOIUrl":"https://doi.org/10.1007/s13105-026-01215-w","url":null,"abstract":"<p><p>The LKB1-AMPK signaling pathway is a central regulator of hepatic energy homeostasis and is increasingly implicated in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). LKB1-mediated AMPK activation promotes fatty acid β-oxidation, autophagy, and mitochondrial biogenesis. At the same time, it suppresses de novo lipogenesis, cholesterol synthesis, and mTOR-dependent anabolic growth, thereby supporting hepatic lipid and energy balance. Impairment of this pathway may disrupt hepatic lipid homeostasis and promote triglyceride accumulation. Oxidative stress, microRNA dysregulation, hormonal imbalance, copper dysregulation, and inflammatory mediators can further contribute to mitochondrial injury, hepatocellular apoptosis, and inflammatory activation. These processes may facilitate progression from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, and hepatocarcinogenesis. LKB1-AMPK signaling also intersects with immunometabolic and stromal pathways. Defects in hepatic immune and stromal compartments may enhance pro-inflammatory Th17 responses and fibrogenic transformation. Therapeutically, pharmacologic activation of LKB1-AMPK has shown context-dependent cytoprotective potential, mainly in preclinical models. Natural compounds, synthetic small molecules, repurposed agents, and nutrient-derived modulators can activate LKB1-AMPK signaling. These interventions reduce steatosis, oxidative stress, and endoplasmic reticulum stress while enhancing autophagic flux and fatty acid catabolism. Additional benefits may arise through gut microbiota-mediated signaling that converges on LKB1-AMPK-dependent metabolic restoration. Overall, the LKB1-AMPK axis links nutrient sensing, mitochondrial function, redox control, and inflammatory regulation in NAFLD pathophysiology. Current evidence supports further development of pathway-targeted interventions, but clinical translation requires stronger human validation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760652","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}