WIREs Mechanisms of Disease最新文献_第7页

The cardiac wound healing response to myocardial infarction. 心肌梗死后心脏伤口愈合的反应。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1584

Upendra Chalise, Mediha Becirovic-Agic, Merry L Lindsey

{"title":"The cardiac wound healing response to myocardial infarction.","authors":"Upendra Chalise, Mediha Becirovic-Agic, Merry L Lindsey","doi":"10.1002/wsbm.1584","DOIUrl":"https://doi.org/10.1002/wsbm.1584","url":null,"abstract":"Myocardial infarction (MI) is defined as evidence of myocardial necrosis consistent with prolonged ischemia. In response to MI, the myocardium undergoes a series of wound healing events that initiate inflammation and shift to anti-inflammation before transitioning to tissue repair that culminates in scar formation to replace the region of the necrotic myocardium. The overall response to MI is determined by two major steps, the first of which is the secretion of proteases by infiltrating leukocytes to breakdown extracellular matrix (ECM) components, a necessary step to remove necrotic cardiomyocytes. The second step is the generation of new ECM that comprises the scar; and this step is governed by the cardiac fibroblasts as the major source of new ECM synthesis. The leukocyte component resides in the middle of the two-step process, contributing to both sides as the leukocytes transition from pro-inflammatory to anti-inflammatory and reparative cell phenotypes. The balance between the two steps determines the final quantity and quality of scar formed, which in turn contributes to chronic outcomes following MI, including the progression to heart failure. This review will summarize our current knowledge regarding the cardiac wound healing response to MI, primarily focused on experimental models of MI in mice. This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology Immune System Diseases > Molecular and Cellular Physiology.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"15 1","pages":"e1584"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d2/3a/WSBM-15-0.PMC10077990.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10642805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Fluids and flows in brain cancer and neurological disorders. 脑癌和神经系统疾病的体液流动。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1582

Peng Jin, Jennifer M Munson

{"title":"Fluids and flows in brain cancer and neurological disorders.","authors":"Peng Jin, Jennifer M Munson","doi":"10.1002/wsbm.1582","DOIUrl":"https://doi.org/10.1002/wsbm.1582","url":null,"abstract":"Interstitial fluid (IF) and cerebrospinal fluid (CSF) are an integral part of the brain, serving to cushion and protect the brain parenchymal cells against damage and aid in their function. The brain IF contains various ions, nutrients, waste products, peptides, hormones, and neurotransmitters. IF moves primarily by pressure-dependent bulk flow through brain parenchyma, draining into the ventricular CSF. The brain ventricles and subarachnoid spaces are filled with CSF which circulates through the perivascular spaces. It also flows into the IF space regulated, in part, by aquaporin channels, removing waste solutes through a process of IF-CSF mixing. During disease development, the composition, flow, and volume of these fluids changes and can lead to brain cell dysfunction. With the improvement of imaging technology and the help of genomic profiling, more information has been and can be obtained from brain fluids; however, the role of CSF and IF in brain cancer and neurobiological disease is still limited. Here we outline recent advances of our knowledge of brain fluid flow in cancer and neurodegenerative disease based on our understanding of its dynamics and composition. This article is categorized under: Cancer > Biomedical Engineering Neurological Diseases > Biomedical Engineering.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"15 1","pages":"e1582"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/dc/89/WSBM-15-0.PMC9869390.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9271944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

CRISPR applications for Duchenne muscular dystrophy: From animal models to potential therapies. CRISPR在杜氏肌营养不良症中的应用:从动物模型到潜在的治疗方法

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1580

Yu C J Chey, Jayshen Arudkumar, Annemieke Aartsma-Rus, Fatwa Adikusuma, Paul Q Thomas

{"title":"CRISPR applications for Duchenne muscular dystrophy: From animal models to potential therapies.","authors":"Yu C J Chey, Jayshen Arudkumar, Annemieke Aartsma-Rus, Fatwa Adikusuma, Paul Q Thomas","doi":"10.1002/wsbm.1580","DOIUrl":"https://doi.org/10.1002/wsbm.1580","url":null,"abstract":"CRISPR gene-editing technology creates precise and permanent modifications to DNA. It has significantly advanced our ability to generate animal disease models for use in biomedical research and also has potential to revolutionize the treatment of genetic disorders. Duchenne muscular dystrophy (DMD) is a monogenic muscle-wasting disease that could potentially benefit from the development of CRISPR therapy. It is commonly associated with mutations that disrupt the reading frame of the DMD gene that encodes dystrophin, an essential scaffolding protein that stabilizes striated muscles and protects them from contractile-induced damage. CRISPR enables the rapid generation of various animal models harboring mutations that closely simulates the wide variety of mutations observed in DMD patients. These models provide a platform for the testing of sequence-specific interventions like CRISPR therapy that aim to reframe or skip DMD mutations to restore functional dystrophin expression. This article is categorized under: Congenital Diseases > Genetics/Genomics/Epigenetics.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"15 1","pages":"e1580"},"PeriodicalIF":3.1,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8b/3e/WSBM-15-0.PMC10078488.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9319968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

PIWI-interacting RNAs and human testicular function. piwi相互作用rna与人类睾丸功能。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-11-01 DOI: 10.1002/wsbm.1572

Gülizar Saritas, Ailsa Maria Main, Sofia Boeg Winge, Nina Mørup, Kristian Almstrup

{"title":"PIWI-interacting RNAs and human testicular function.","authors":"Gülizar Saritas, Ailsa Maria Main, Sofia Boeg Winge, Nina Mørup, Kristian Almstrup","doi":"10.1002/wsbm.1572","DOIUrl":"https://doi.org/10.1002/wsbm.1572","url":null,"abstract":"Small noncoding RNAs (sncRNAs) are pieces of RNA with a length below 200 bp and represent a diverse group of RNAs having many different biological functions. The best described subtype is the microRNAs which primarily function in posttranscriptional gene regulation and appear essential for most physiological processes. Of particular interest for the germline is the PIWI-interacting RNAs (piRNAs) which are a class of sncRNA of 21-35 bp in length that are almost exclusively found in germ cells. Recently, it has become clear that piRNAs are essential for testicular function, and in this perspective, we outline the current knowledge of piRNAs in humans. Although piRNAs appear unique to germ cells, they have also been described in various somatic cancers and biofluids. Here, we discuss the potential function of piRNAs in somatic tissues and whether detection in biofluids may be used as a biomarker for testicular function. This article is categorized under: Reproductive System Diseases > Genetics/Genomics/Epigenetics Reproductive System Diseases > Molecular and Cellular Physiology.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 6","pages":"e1572"},"PeriodicalIF":3.1,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9788060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10436816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Mechanisms of immune effector cell-associated neurotoxicity syndrome after CAR-T treatment. CAR-T治疗后免疫效应细胞相关神经毒性综合征的机制。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-11-01 DOI: 10.1002/wsbm.1576

Tianning Gu, Kejia Hu, Xiaohui Si, Yongxian Hu, He Huang

{"title":"Mechanisms of immune effector cell-associated neurotoxicity syndrome after CAR-T treatment.","authors":"Tianning Gu, Kejia Hu, Xiaohui Si, Yongxian Hu, He Huang","doi":"10.1002/wsbm.1576","DOIUrl":"https://doi.org/10.1002/wsbm.1576","url":null,"abstract":"Chimeric antigen receptor T-cell (CAR-T) treatment has revolutionized the landscape of cancer therapy with significant efficacy on hematologic malignancy, especially in relapsed and refractory B cell malignancies. However, unexpected serious toxicities such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) still hamper its broad application. Clinical trials using CAR-T cells targeting specific antigens on tumor cell surface have provided valuable information about the characteristics of ICANS. With unclear mechanism of ICANS after CAR-T treatment, unremitting efforts have been devoted to further exploration. Clinical findings from patients with ICANS strongly indicated existence of overactivated peripheral immune response followed by endothelial activation-induced blood-brain barrier (BBB) dysfunction, which triggers subsequent central nervous system (CNS) inflammation and neurotoxicity. Several animal models have been built but failed to fully replicate the whole spectrum of ICANS in human. Hopefully, novel and powerful technologies like single-cell analysis may help decipher the precise cellular response within CNS from a different perspective when ICANS happens. Moreover, multidisciplinary cooperation among the subjects of immunology, hematology, and neurology will facilitate better understanding about the complex immune interaction between the peripheral, protective barriers, and CNS in ICANS. This review elaborates recent findings about ICANS after CAR-T treatment from bed to bench, and discusses the potential cellular and molecular mechanisms that may promote effective management in the future. This article is categorized under: Cancer > Biomedical Engineering Immune System Diseases > Molecular and Cellular Physiology Neurological Diseases > Molecular and Cellular Physiology.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 6","pages":"e1576"},"PeriodicalIF":3.1,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1b/d8/WSBM-14-e1576.PMC9787013.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10446991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Molecular mechanisms underlying bacterial resistance to ceftazidime/avibactam. 细菌对头孢他啶/阿维巴坦耐药的分子机制

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-11-01 DOI: 10.1002/wsbm.1571

Luying Xiong, Xueting Wang, Yuan Wang, Wei Yu, Yanzi Zhou, Xiaohui Chi, Tingting Xiao, Yonghong Xiao

{"title":"Molecular mechanisms underlying bacterial resistance to ceftazidime/avibactam.","authors":"Luying Xiong, Xueting Wang, Yuan Wang, Wei Yu, Yanzi Zhou, Xiaohui Chi, Tingting Xiao, Yonghong Xiao","doi":"10.1002/wsbm.1571","DOIUrl":"https://doi.org/10.1002/wsbm.1571","url":null,"abstract":"Ceftazidime/avibactam (CAZ/AVI), a combination of ceftazidime and a novel β-lactamase inhibitor (avibactam) that has been approved by the U.S. Food and Drug Administration, the European Union, and the National Regulatory Administration in China. CAZ/AVI is used mainly to treat complicated urinary tract infections and complicated intra-abdominal infections in adults, as well as to treat patients infected with Carbapenem-resistant Enterobacteriaceae (CRE) susceptible to CAZ/AVI. However, increased clinical application of CAZ/AVI has resulted in the development of resistant strains. Mechanisms of resistance in most of these strains have been attributed to blaKPC mutations, which lead to amino acid substitutions in β-lactamase and changes in gene expression. Resistance to CAZ/AVI is also associated with reduced expression and loss of outer membrane proteins or overexpression of efflux pumps. In this review, the prevalence of CAZ/AVI-resistance bacteria, resistance mechanisms, and selection of detection methods of CAZ/AVI are demonstrated, aiming to provide scientific evidence for the clinical prevention and treatment of CAZ/AVI resistant strains, and provide guidance for the development of new drugs. This article is categorized under: Infectious Diseases > Molecular and Cellular Physiology.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 6","pages":"e1571"},"PeriodicalIF":3.1,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9788277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10445244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

A compendium of validated pain genes. 一个经过验证的疼痛基因纲要。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-11-01 DOI: 10.1002/wsbm.1570

Eric Wistrom, Rebecca Chase, Patrick R Smith, Zachary T Campbell

{"title":"A compendium of validated pain genes.","authors":"Eric Wistrom, Rebecca Chase, Patrick R Smith, Zachary T Campbell","doi":"10.1002/wsbm.1570","DOIUrl":"https://doi.org/10.1002/wsbm.1570","url":null,"abstract":"The development of novel pain therapeutics hinges on the identification and rigorous validation of potential targets. Model organisms provide a means to test the involvement of specific genes and regulatory elements in pain. Here we provide a list of genes linked to pain-associated behaviors. We capitalize on results spanning over three decades to identify a set of 242 genes. They support a remarkable diversity of functions spanning action potential propagation, immune response, GPCR signaling, enzymatic catalysis, nucleic acid regulation, and intercellular signaling. Making use of existing tissue and single-cell high-throughput RNA sequencing datasets, we examine their patterns of expression. For each gene class, we discuss archetypal members, with an emphasis on opportunities for additional experimentation. Finally, we discuss how powerful and increasingly ubiquitous forward genetic screening approaches could be used to improve our ability to identify pain genes. This article is categorized under: Neurological Diseases > Genetics/Genomics/Epigenetics Neurological Diseases > Molecular and Cellular Physiology.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 6","pages":"e1570"},"PeriodicalIF":3.1,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9787016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10436299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Pathogenesis of neural tube defects: The regulation and disruption of cellular processes underlying neural tube closure. 神经管缺陷的发病机制:神经管闭合背后的细胞过程的调节和破坏。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-09-01 DOI: 10.1002/wsbm.1559

David M Engelhardt, Cara A Martyr, Lee Niswander

{"title":"Pathogenesis of neural tube defects: The regulation and disruption of cellular processes underlying neural tube closure.","authors":"David M Engelhardt, Cara A Martyr, Lee Niswander","doi":"10.1002/wsbm.1559","DOIUrl":"https://doi.org/10.1002/wsbm.1559","url":null,"abstract":"Neural tube closure (NTC) is crucial for proper development of the brain and spinal cord and requires precise morphogenesis from a sheet of cells to an intact three-dimensional structure. NTC is dependent on successful regulation of hundreds of genes, a myriad of signaling pathways, concentration gradients, and is influenced by epigenetic and environmental cues. Failure of NTC is termed a neural tube defect (NTD) and is a leading class of congenital defects in the United States and worldwide. Though NTDs are all defined as incomplete closure of the neural tube, the pathogenesis of an NTD determines the type, severity, positioning, and accompanying phenotypes. In this review, we survey pathogenesis of NTDs relating to disruption of cellular processes arising from genetic mutations, altered epigenetic regulation, and environmental influences by micronutrients and maternal condition. This article is categorized under: Congenital Diseases > Genetics/Genomics/Epigenetics Neurological Diseases > Genetics/Genomics/Epigenetics Neurological Diseases > Stem Cells and Development.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 5","pages":"e1559"},"PeriodicalIF":3.1,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9605354/pdf/nihms-1799087.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10134712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

New developments in the biology of fibroblast growth factors. 成纤维细胞生长因子生物学的新进展。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-07-01 DOI: 10.1002/wsbm.1549

David M Ornitz, Nobuyuki Itoh

{"title":"New developments in the biology of fibroblast growth factors.","authors":"David M Ornitz, Nobuyuki Itoh","doi":"10.1002/wsbm.1549","DOIUrl":"https://doi.org/10.1002/wsbm.1549","url":null,"abstract":"The fibroblast growth factor (FGF) family is composed of 18 secreted signaling proteins consisting of canonical FGFs and endocrine FGFs that activate four receptor tyrosine kinases (FGFRs 1-4) and four intracellular proteins (intracellular FGFs or iFGFs) that primarily function to regulate the activity of voltage-gated sodium channels and other molecules. The canonical FGFs, endocrine FGFs, and iFGFs have been reviewed extensively by us and others. In this review, we briefly summarize past reviews and then focus on new developments in the FGF field since our last review in 2015. Some of the highlights in the past 6 years include the use of optogenetic tools, viral vectors, and inducible transgenes to experimentally modulate FGF signaling, the clinical use of small molecule FGFR inhibitors, an expanded understanding of endocrine FGF signaling, functions for FGF signaling in stem cell pluripotency and differentiation, roles for FGF signaling in tissue homeostasis and regeneration, a continuing elaboration of mechanisms of FGF signaling in development, and an expanding appreciation of roles for FGF signaling in neuropsychiatric diseases. This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology Neurological Diseases > Molecular and Cellular Physiology Congenital Diseases > Stem Cells and Development Cancer > Stem Cells and Development.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"14 4","pages":"e1549"},"PeriodicalIF":3.1,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10115509/pdf/nihms-1890656.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 42

Transition to extrauterine life and the modeling of perinatal asphyxia in rats. 大鼠向宫外生活的过渡和围产期窒息的建模。

IF 3.1 3区医学

WIREs Mechanisms of Disease Pub Date : 2022-06-16 DOI: 10.1002/wsbm.1568

M. Ortiz, F. Loidl, Pablo Vázquez-Borsetti

{"title":"Transition to extrauterine life and the modeling of perinatal asphyxia in rats.","authors":"M. Ortiz, F. Loidl, Pablo Vázquez-Borsetti","doi":"10.1002/wsbm.1568","DOIUrl":"https://doi.org/10.1002/wsbm.1568","url":null,"abstract":"Generation of murine models for the study of birth-related pathologies has proven to be a complex and controversial problem. Differences in the relative timing of developmental events of both species have led some researchers to suggest that the rat is born comparatively less developed than the human. The solution proposed to this problem would consist in the delay of the experiments of perinatal asphyxia (PA), usually up to 7-10 days, allowing developmental levels to \"equalize\" with the human at birth. This solution generates a new set of problems. The developmental milestones in both species follow a divergent temporal pattern. Increasing the age of the rat not only can improve resemblance with humans but also will make the model miss a crucial set of milestones related to birth. During this process, there are specific mechanisms to protect the fetus from neuronal damage, especially those caused by asphyxia. These factors are not present in models where the asphyxia is delayed. In these models, there will be more false positives and more damage that would not be present in humans exposed to PA. This article is categorized under: Cancer > Stem Cells and Development Congenital Diseases > Environmental Factors Neurological Diseases > Environmental Factors.","PeriodicalId":29896,"journal":{"name":"WIREs Mechanisms of Disease","volume":"1 1","pages":"e1568"},"PeriodicalIF":3.1,"publicationDate":"2022-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49363888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1