Free Radical Research最新文献_第4页

Hyperoxia induces autophagy in pulmonary epithelial cells: insights from in vivo and in vitro experiments. 高氧诱导肺上皮细胞自噬：来自体内和体外实验的见解。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-02 DOI: 10.1080/10715762.2024.2446321

Kuo-Tsang Huang, Wen-Hui Tsai, Chih-Wei Chen, Yea-Shwu Hwang, Hung-Chi Cheng, Chin-Wei Yeh, Yuan-Ho Lin, An-Jie Cheng, Hao-Chun Chang, Shio-Jean Lin, Meng-Chi Yen, Wen-Tsan Chang

{"title":"Hyperoxia induces autophagy in pulmonary epithelial cells: insights from in vivo and in vitro experiments.","authors":"Kuo-Tsang Huang, Wen-Hui Tsai, Chih-Wei Chen, Yea-Shwu Hwang, Hung-Chi Cheng, Chin-Wei Yeh, Yuan-Ho Lin, An-Jie Cheng, Hao-Chun Chang, Shio-Jean Lin, Meng-Chi Yen, Wen-Tsan Chang","doi":"10.1080/10715762.2024.2446321","DOIUrl":"10.1080/10715762.2024.2446321","url":null,"abstract":"Patients with hypoxemia require high-concentration oxygen therapy. However, prolonged exposure to oxygen concentrations 21% higher than physiological concentrations (hyperoxia) may cause oxidative cellular damage. Pulmonary alveolar epithelial cells are major targets for hyperoxia-induced oxidative stress. In this study, we evaluated the therapeutic potential of the antioxidant N-acetyl-L-cysteine (NAC) for preventing hyperoxia-induced cell death. In vitro experiments were performed using the human lung cancer cell line A549. In brief, NAC-treated and untreated cells were exposed to various concentrations of oxygen (hyperoxia) for different durations. The results indicated that hyperoxia inhibited proliferation and caused cell cycle arrest in A549 cells. It also induced necrosis and autophagy. Furthermore, hyperoxia increased intracellular reactive oxygen species levels and altered mitochondrial membrane potential. Co-treatment with NAC improved the survival of cells exposed to 95% oxygen for 24 h. Experiments performed using a neonatal rat model of acute lung injury confirmed that hyperoxia induced an autophagic response. This study provides evidence for hyperoxia-induced autophagy both in vitro and in vivo. NAC can protect A549 cells from death induced by short-term hyperoxia. Our findings may inform protective strategies against hyperoxia-induced injury in developing lungs-for example, bronchopulmonary dysplasia in premature infants.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"9-22"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876700","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}

引用次数: 0

Anti-oxidants as therapeutic agents for oxidative stress associated pathologies: future challenges and opportunities. 抗氧化剂作为氧化应激相关病理的治疗剂：未来的挑战和机遇。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-10 DOI: 10.1080/10715762.2025.2450504

Shivani R Nandha, Rahul Checker, Raghavendra S Patwardhan, Deepak Sharma, Santosh K Sandur

{"title":"Anti-oxidants as therapeutic agents for oxidative stress associated pathologies: future challenges and opportunities.","authors":"Shivani R Nandha, Rahul Checker, Raghavendra S Patwardhan, Deepak Sharma, Santosh K Sandur","doi":"10.1080/10715762.2025.2450504","DOIUrl":"10.1080/10715762.2025.2450504","url":null,"abstract":"Free radicals have been implicated in the pathogenesis of cancer along with cardiovascular, neurodegenerative, pulmonary and inflammatory disorders. Further, the relationship between oxidative stress and disease is distinctively established. Clinical trials using anti-oxidants for the prevention of disease progression have indicated some beneficial effects. However, these trials failed to establish anti-oxidants as therapeutic agents due to lack of efficacy. This is attributed to the fact that living systems are under dynamic redox control wherein their redox behavior is compartmentalized and simple aggregation of redox couples, distributed throughout the system, is of miniscule importance while determining their overall redox state. Further, free radical metabolism is intriguingly complex as they play plural roles segregated in a spatio-temporal manner. Depending on quality, quantity and site of generation, free radicals exhibit beneficial or harmful effects. Use of nonspecific, non-targeted, general ROS scavengers lead to systemic elimination of all types of ROS and interferes in cellular signaling. Failure of anti-oxidants to act as therapeutic agents lies in this oversimplification of extremely dynamic cellular redox environment as a static and non-compartmentalized redox state. Rather than generalizing the term \"oxidative stress\" if we can identify the \"type of oxidative stress\" in different types of diseases, a targeted and more specific anti-oxidant therapy may be developed. In this review, we discuss the concept of redox dynamics, role and type of oxidative stress in disease conditions, and current status of anti-oxidants as therapeutic agents. Further, we probe the possibility of developing novel, targeted and efficacious anti-oxidants with drug-like properties.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"61-85"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947361","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}

引用次数: 0

NADPH oxidase derived ROS promote arterial contraction in early postnatal rats by activation of L-type voltage-gated Ca²⁺ channels. NADPH氧化酶衍生的ROS通过激活l型电压门控Ca2+通道促进出生后早期大鼠动脉收缩。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2024-12-30 DOI: 10.1080/10715762.2024.2448483

Anastasia A Shvetsova, Valentina S Shateeva, Margarita A Khlystova, Yulia A Makukha, Olga S Tarasova, Dina K Gaynullina

{"title":"NADPH oxidase derived ROS promote arterial contraction in early postnatal rats by activation of L-type voltage-gated Ca2+ channels.","authors":"Anastasia A Shvetsova, Valentina S Shateeva, Margarita A Khlystova, Yulia A Makukha, Olga S Tarasova, Dina K Gaynullina","doi":"10.1080/10715762.2024.2448483","DOIUrl":"10.1080/10715762.2024.2448483","url":null,"abstract":"Reactive oxygen species (ROS) produced by NADPH oxidase promote contraction of peripheral arteries, which is especially pronounced in early postnatal period in comparison to adulthood, but the mechanisms of such vasomotor influence are poorly understood. We tested the hypothesis that Rho-kinase and protein kinase C (PKC) mediate procontractile influence of NADPH oxidase derived ROS in peripheral artery of early postnatal rats. In addition, we evaluated the involvement Src-kinase and L-type voltage-gated Ca2+ channels (LTCC) into procontractile influence of ROS, produced by NADPH oxidase, because of their known interplay with Rho-kinase and PKC pathways. Saphenous arteries from 11- to 15-day-old male rats were studied using quantitative PCR, isometric myography and lucigenin-enhanced chemiluminescence. Arterial tissue of early postnatal rats contained Nox2, Nox4, Duox1 and Duox2 mRNAs, among which Nox2 mRNA was the most abundant. Pan-NADPH oxidase inhibitor VAS2870 (10 µM) significantly reduced arterial contractile responses to methoxamine. The inhibitors of Rho-kinase (Y27632, 3 µM), PKC (GF109203X, 10 µM) and Src-kinase (PP2, 10 µM), as well as LTCC blockers (nimodipine, 0.1 µM, and verapamil, 0.1 μM) also reduced methoxamine-induced contraction. Importantly, the effect of VAS2870 persisted in the presence of Rho-kinase, PKC or Src-kinase inhibitors, but not in the presence of LTCC blocker. Notably, the blockade of LTCC did not affect either basal or NADPH-induced O2•- production. Our data show that LTCC, but not Rho-kinase, PKC or Src-kinase are involved into procontractile effect of ROS, produced by NADPH oxidase, in saphenous artery of young rats. Сalcium influx through LTCC does not activate ROS production by NADPH oxidase.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":"59 1","pages":"49-60"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064676","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}

引用次数: 0

Identification of narciclasine as a novel NRF2 inhibitor. 新型NRF2抑制剂水仙精的鉴定。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-15 DOI: 10.1080/10715762.2025.2451679

Hoang Hai Ngo, Bo-Yeung Yu, Jeong-Eun Lee, Hyunwoo Kim, Young-Sam Keum

引用次数: 0

Exploring the impact of Apelin and Reactive Oxygen Species on autophagy and cell senescence in pre-eclampsia. 探讨Apelin和活性氧对子痫前期自噬和细胞衰老的影响。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-07 DOI: 10.1080/10715762.2024.2446337

Xue Peng, Xi Tan, Li Dai, Wei Xia, Zhao Wu

引用次数: 0

Modulation of inflammatory signaling by vitamin E metabolites and its therapeutic implications. 维生素E代谢产物对炎症信号的调节及其治疗意义。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2025-01-01 Epub Date: 2025-01-08 DOI: 10.1080/10715762.2024.2449457

Seher Mese-Tayfur, Tugce Demirel-Yalcıner, Anna Migni, Desirée Bartolini, Francesco Galli, Nesrin Kartal Ozer, Erdi Sozen

{"title":"Modulation of inflammatory signaling by vitamin E metabolites and its therapeutic implications.","authors":"Seher Mese-Tayfur, Tugce Demirel-Yalcıner, Anna Migni, Desirée Bartolini, Francesco Galli, Nesrin Kartal Ozer, Erdi Sozen","doi":"10.1080/10715762.2024.2449457","DOIUrl":"10.1080/10715762.2024.2449457","url":null,"abstract":"Naturally occurring vitamin E is a lipophilic plant-derived molecule corresponding to the 2 R forms of alpha-tocopherol. A series of natural analogs or tocochromanols are present in nature, including β-, γ- and δ-tocopherol (βT, γT, δT), the corresponding tocotrienols (αTE, βTE, γTE, δTE) and tocomonoenols. Differences between these analogs as lipophilic antioxidants and modulators of molecular processes suggest specific therapeutic properties against various disorders associated with acute and chronic inflammation. However, hepatic metabolism of these compounds via cytochrome P450-initiated side chain ω-oxidation involves the production of long-chain metabolites (LCMs) followed by intermediate (ICMs) and short-chain metabolites (SCMs), respectively. Despite the initial studies indicating these metabolites as catabolic-end products, recent findings identify their importance in providing biological functions. In this scope, LCMs, especially 13'-carboxychromanols (13'-COOHs), have been reported to hold stronger anti-inflammatory capacity than their unmetabolized precursors due to their ability to inhibit 5-lipoxygenase and cyclooxygenase-catalyzed eicosanoid formation, as well as their modulation of the pro-inflammatory transcriptional protein nuclear factor κB (NF-κB). Also, these LCMs have been reported to enhance detoxification and lipid metabolism pathways associated with cellular inflammation by modulating the nuclear receptors peroxisome proliferator-activated receptor-γ (PPARγ) and pregnane x receptor (PXR). These properties of LCMs will be described in this narrative review article focusing on recent information regarding their bioavailability, anti-inflammatory effects, and mechanisms of action in acute and chronic inflammatory disorders.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":"59 1","pages":"86-101"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143055904","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}

引用次数: 0

Apelin deficiency exacerbates cardiac injury following infarction by accelerating cardiomyocyte ferroptosis. Apelin缺乏通过加速心肌细胞铁下垂加重心肌梗死后的心脏损伤。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-12-01 Epub Date: 2024-12-28 DOI: 10.1080/10715762.2024.2443606

Yuechu Zhao, Xiaoting Liang, Ting Li, Zhuang Shao, Zhi Cao, Yi Zeng, Xiaofei Yan, Qi Chen, Hao Zhou, Weifeng Li, Guifen Cheng, Yaping Jiang, Xin Li, Yuelin Zhang, Bei Hu

{"title":"Apelin deficiency exacerbates cardiac injury following infarction by accelerating cardiomyocyte ferroptosis.","authors":"Yuechu Zhao, Xiaoting Liang, Ting Li, Zhuang Shao, Zhi Cao, Yi Zeng, Xiaofei Yan, Qi Chen, Hao Zhou, Weifeng Li, Guifen Cheng, Yaping Jiang, Xin Li, Yuelin Zhang, Bei Hu","doi":"10.1080/10715762.2024.2443606","DOIUrl":"10.1080/10715762.2024.2443606","url":null,"abstract":"Apelin is an endogenous ligand for the Apelin receptor and is a critical protective effector in myocardial infarction (MI). Nevertheless, these protective mechanisms are not fully understood. Ferroptosis is the major driving factor of MI. This study aimed to investigate the effects and underlying regulatory mechanisms of Apelin on cardiomyocyte ferroptosis in MI. A model of MI was induced in adult C57BL/6J wild type (WT) and Apelin knockout (Apelin-/-) mice. Cardiac function was examined by echocardiography 4 weeks post-MI. RNA-seq, histochemical analyses, and Western blotting were applied to examine the effects of Apelin knockout on the transcriptome and pathological remodeling following infarction and the molecular mechanisms. Mice neonatal cardiomyocytes (NCMs) were used to establish the serum deprivation/hypoxia (SD/H) model in vitro. Compared with WT mice, Apelin-/- mice exhibited more severe impairment of cardiac function and increased fibrosis following infarction. Transcriptome and biochemical analyses revealed the involvement of ferroptosis in mediating Apelin function in MI. Ferroptosis-related proteins were significantly increased post-MI in Apelin-/- mice whereas p-AMPK was greatly decreased. Apelin treatment activated the AMPK pathway and thereby inhibited ferroptosis of NCMs induced by SD/H in vitro. These protective effects were partially reversed by AMPK inhibitor. Apelin deficiency aggravated cardiac dysfunction following infarction by activating cardiomyocyte ferroptosis via inhibition of the AMPK pathway. This offers a novel potential therapeutic target for MI treatment.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"854-867"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893271","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}

引用次数: 0

Theoretical studies on the antioxidant activity of potential marine xanthones. 关于潜在海洋氧杂蒽酮抗氧化活性的理论研究。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-12-01 Epub Date: 2024-12-15 DOI: 10.1080/10715762.2024.2438918

Phan Thi Thuy, Nguyen Xuan Ha

{"title":"Theoretical studies on the antioxidant activity of potential marine xanthones.","authors":"Phan Thi Thuy, Nguyen Xuan Ha","doi":"10.1080/10715762.2024.2438918","DOIUrl":"10.1080/10715762.2024.2438918","url":null,"abstract":"In this study, a quantum chemical exploration was conducted to assess the antioxidant activity of xanthones isolated from marine sources, focusing on thermodynamics and kinetics within simulated physiological environments. DFT analysis revealed that xanthones such as 1,4,7-trihydroxy-6-methylxanthone (1), 1,4,5-trihydroxy-2-methylxanthone (2), arthone C (3), 2,3,4,6,8-pentahydroxy-1-methylxanthone (4), sterigmatocystin (5), oxisterigmatocystin C (6), and oxisterigmatocystin D (7) favor the SPLET pathway in water and the FHT pathway in lipid environments. The kinetic study of these xanthones reacting with the hydroperoxyl radical (HOO•) was conducted using the formal hydrogen atom transfer (FHT) mechanism and the single electron transfer (SET) mechanism. The results showed that compounds 1-4 exhibited antioxidant activities in aqueous environments surpassing that of the reference compound Trolox, with rate constants ranging from 2.02 x 105 to 9.44 x 107 M-1·s-1. In lipid environments, compounds 1 and 2 also demonstrated higher rate constants than Trolox. Additionally, molecular docking and molecular dynamics analysis suggested that xanthones 1-7 potentially inhibit the pro-oxidant effect of the Keap1 enzyme, highlighting their promise as both antiradicals and enzyme inhibitors.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"826-840"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827681","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}

引用次数: 0

New era of plasma dentistry. 等离子牙科的新时代。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-12-01 Epub Date: 2024-12-27 DOI: 10.1080/10715762.2024.2446323

Kotaro Sato, Hiromasa Tanaka, Yasumasa Okazaki, Masaru Hori, Hideharu Hibi, Shinya Toyokuni

{"title":"New era of plasma dentistry.","authors":"Kotaro Sato, Hiromasa Tanaka, Yasumasa Okazaki, Masaru Hori, Hideharu Hibi, Shinya Toyokuni","doi":"10.1080/10715762.2024.2446323","DOIUrl":"10.1080/10715762.2024.2446323","url":null,"abstract":"Plasma, which was coined by Irving Langmuir in 1928, is the fourth physical state after the solid/liquid/gas phases. Low-temperature plasma (LTP) is a contradictory condition that involves high energy with free radicals at near-body temperatures and was developed through engineering in the 1990's. Research on LTP in engineering and medical fields has rapidly developed since the 2000's. LTP can be applied through direct or indirect exposure, and there are advantages to both methods. In the medical field, LTP has been found to exert several effects, such as wound healing, hemostasis and anticancer effects, mainly based on different levels of oxidative stress. In the dental field, studies have been performed on LTP applications for general dental procedures, such as restorative, periodontal and prosthodontic procedures, and for oral cancer treatment. Many studies have demonstrated the effectiveness of LTP. Compared with other organs, the anatomical characteristic of the oral cavity is easy direct observation, which is highly advantageous for clinical applications. Due to its good accessibility and efficiency, plasma dentistry is expected to be applied to various dental applications in clinics in the near future.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"868-874"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876702","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}

引用次数: 0

Urban aerosol particulate matter promotes cellular senescence through mitochondrial ROS-mediated Akt/Nrf2 downregulation in human retinal pigment epithelial cells. 城市气溶胶颗粒物通过线粒体ros介导的Akt/Nrf2下调促进人视网膜色素上皮细胞衰老。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-12-01 Epub Date: 2024-12-08 DOI: 10.1080/10715762.2024.2438919

Beom Su Park, EunJin Bang, Hyun Hwangbo, Gi-Young Kim, JaeHun Cheong, Yung Hyun Choi

{"title":"Urban aerosol particulate matter promotes cellular senescence through mitochondrial ROS-mediated Akt/Nrf2 downregulation in human retinal pigment epithelial cells.","authors":"Beom Su Park, EunJin Bang, Hyun Hwangbo, Gi-Young Kim, JaeHun Cheong, Yung Hyun Choi","doi":"10.1080/10715762.2024.2438919","DOIUrl":"10.1080/10715762.2024.2438919","url":null,"abstract":"Urban aerosol particulate matter (UPM) is widespread in the environment, and its concentration continues to increase. Several recent studies have reported that UPM results in premature cellular senescence, but few studies have investigated the molecular basis of UPM-induced senescence in retinal pigment epithelial (RPE) cells. In this study, we primarily evaluated UPM-induced premature senescence and the protective function of nuclear factor erythroid 2-related factor 2 (Nrf2) in human RPE ARPE-19 cells. The findings indicated that UPM exposure substantially induced premature cellular senescence in ARPE-19 cells, as observed by increased β-galactosidase activity, expression levels of senescence-associated marker proteins, and senescence-associated phenotypes. Such UPM-induced senescence is associated with mitochondrial oxidative stress-mediated phosphatidylinositol 3'-kinase/Akt/Nrf2 downregulation. Sulforaphane-mediated Nrf2 activation Sulforaphane-mediated upregulation of phosphorylated Nrf2 suppressed the decrease in its target antioxidant gene, NAD(P)H quinone oxidoreductase 1, under UPM, which notably prevented ARPE-19 cells from UPM-induced cellular senescence. By contrast, Nrf2 knockdown exacerbated cellular senescence and promoted oxidative stress. Collectively, our results demonstrate the regulatory role of Nrf2 in UPM-induced senescence of RPE cells and suggest that Nrf2 is a potential molecular target.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":" ","pages":"841-853"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794468","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}

引用次数: 0