Pub Date : 2024-12-18DOI: 10.1038/s41581-024-00920-3
Deirdre Sawinski, Marshall J. Glesby
New data demonstrate that in people with HIV infection, transplantation outcomes with HIV-positive donor kidneys are not inferior to those with HIV-negative donor kidneys and donor-derived HIV strains do not persist in the recipients. This approach should be standard of care for kidney transplantation in people living with HIV.
{"title":"Dare to HOPE: a step closer to HIV+-to-HIV+ kidney transplantation as standard of care","authors":"Deirdre Sawinski, Marshall J. Glesby","doi":"10.1038/s41581-024-00920-3","DOIUrl":"https://doi.org/10.1038/s41581-024-00920-3","url":null,"abstract":"New data demonstrate that in people with HIV infection, transplantation outcomes with HIV-positive donor kidneys are not inferior to those with HIV-negative donor kidneys and donor-derived HIV strains do not persist in the recipients. This approach should be standard of care for kidney transplantation in people living with HIV.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"1 1","pages":""},"PeriodicalIF":41.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142841074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-18DOI: 10.1038/s41581-024-00921-2
Lauren Heath, Carol Pollock
Sodium–glucose co-transporter 2 inhibitors have revolutionized the management of chronic kidney disease. However, long-term data regarding their use are lacking. The post-trial follow-up study to EMPA-KIDNEY provides several insights into how the effects of these powerful medications might be optimized, but several key questions remain unanswered.
{"title":"Long-term lessons from EMPA-KIDNEY","authors":"Lauren Heath, Carol Pollock","doi":"10.1038/s41581-024-00921-2","DOIUrl":"https://doi.org/10.1038/s41581-024-00921-2","url":null,"abstract":"Sodium–glucose co-transporter 2 inhibitors have revolutionized the management of chronic kidney disease. However, long-term data regarding their use are lacking. The post-trial follow-up study to EMPA-KIDNEY provides several insights into how the effects of these powerful medications might be optimized, but several key questions remain unanswered.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"11 1","pages":""},"PeriodicalIF":41.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142848925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-16DOI: 10.1038/s41581-024-00919-w
Shen Li, Katalin Susztak
Diabetic kidney disease (DKD), the most common cause of chronic kidney disease, is primarily caused by metabolic dysfunction, likely due to mitochondrial abnormalities. In 2024, several studies made important strides towards defining the molecular mechanisms that underlie the development of DKD.
{"title":"Mitochondrial dysfunction has a central role in diabetic kidney disease","authors":"Shen Li, Katalin Susztak","doi":"10.1038/s41581-024-00919-w","DOIUrl":"10.1038/s41581-024-00919-w","url":null,"abstract":"Diabetic kidney disease (DKD), the most common cause of chronic kidney disease, is primarily caused by metabolic dysfunction, likely due to mitochondrial abnormalities. In 2024, several studies made important strides towards defining the molecular mechanisms that underlie the development of DKD.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 2","pages":"77-78"},"PeriodicalIF":28.6,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142825494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-12DOI: 10.1038/s41581-024-00923-0
Colin Reily, Tyler J. Stewart, Matthew B. Renfrow, Jan Novak
{"title":"Publisher Correction: Glycosylation in health and disease","authors":"Colin Reily, Tyler J. Stewart, Matthew B. Renfrow, Jan Novak","doi":"10.1038/s41581-024-00923-0","DOIUrl":"10.1038/s41581-024-00923-0","url":null,"abstract":"","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 3","pages":"216-216"},"PeriodicalIF":28.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41581-024-00923-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-12DOI: 10.1038/s41581-024-00915-0
Myung-Gyu Kim (, ), Sang Kyung Jo (, )
Inter-organ interactions are critical for homeostasis and proper organ functioning. Several studies published in 2024 have provided insights into the mechanisms underlying reciprocal interactions of the kidney with the brain, gut and liver.
{"title":"New insights into kidney crosstalk with distant organs","authors":"Myung-Gyu Kim \u0000 (, ), Sang Kyung Jo \u0000 (, )","doi":"10.1038/s41581-024-00915-0","DOIUrl":"10.1038/s41581-024-00915-0","url":null,"abstract":"Inter-organ interactions are critical for homeostasis and proper organ functioning. Several studies published in 2024 have provided insights into the mechanisms underlying reciprocal interactions of the kidney with the brain, gut and liver.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 2","pages":"73-74"},"PeriodicalIF":28.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-10DOI: 10.1038/s41581-024-00910-5
Iain L. C. Chapple, Josefine Hirschfeld, Paul Cockwell, Thomas Dietrich, Praveen Sharma
Periodontitis is a ubiquitous chronic inflammatory disease affecting the supporting tissues of the teeth and is a major cause of multiple tooth loss. Despite being preventable, periodontitis and dental caries are responsible for more years lost to disability than any other human condition. The most severe form of periodontitis affects 1 billion individuals, and its prevalence is increasing globally. Periodontitis arises from a dysregulated and hyperactive inflammatory response to dysbiosis in the periodontal microbiome. This response has systemic effects associated with premature mortality and elevated risk of several systemic non-communicable diseases (NCDs), including atheromatous cardiovascular disease, type 2 diabetes and chronic kidney disease (CKD). This risk association between periodontitis and NCDs is independent of their shared common risk factors, suggesting that periodontitis is a non-traditional risk factor for NCDs such as CKD. As periodontitis progresses, the immune cells and mediators underpinning its pathophysiology leak into the systemic circulation through the ulcerated oral mucosal lining, inducing in a systemic inflammatory profile that closely mirrors that observed in patients with CKD. The relationship between periodontitis and CKD seems to be bi-directional, but large-scale intervention studies are required to clarify causality and could lead to new care pathways for managing each condition as an exposure for the other.
{"title":"Interplay between periodontitis and chronic kidney disease","authors":"Iain L. C. Chapple, Josefine Hirschfeld, Paul Cockwell, Thomas Dietrich, Praveen Sharma","doi":"10.1038/s41581-024-00910-5","DOIUrl":"https://doi.org/10.1038/s41581-024-00910-5","url":null,"abstract":"<p>Periodontitis is a ubiquitous chronic inflammatory disease affecting the supporting tissues of the teeth and is a major cause of multiple tooth loss. Despite being preventable, periodontitis and dental caries are responsible for more years lost to disability than any other human condition. The most severe form of periodontitis affects 1 billion individuals, and its prevalence is increasing globally. Periodontitis arises from a dysregulated and hyperactive inflammatory response to dysbiosis in the periodontal microbiome. This response has systemic effects associated with premature mortality and elevated risk of several systemic non-communicable diseases (NCDs), including atheromatous cardiovascular disease, type 2 diabetes and chronic kidney disease (CKD). This risk association between periodontitis and NCDs is independent of their shared common risk factors, suggesting that periodontitis is a non-traditional risk factor for NCDs such as CKD. As periodontitis progresses, the immune cells and mediators underpinning its pathophysiology leak into the systemic circulation through the ulcerated oral mucosal lining, inducing in a systemic inflammatory profile that closely mirrors that observed in patients with CKD. The relationship between periodontitis and CKD seems to be bi-directional, but large-scale intervention studies are required to clarify causality and could lead to new care pathways for managing each condition as an exposure for the other.</p>","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"29 1","pages":""},"PeriodicalIF":41.5,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142797028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-06DOI: 10.1038/s41581-024-00907-0
Agnes B. Fogo, Raymond C. Harris
Models of kidney injury have classically concentrated on glomeruli as the primary site of injury leading to glomerulosclerosis or on tubules as the primary site of injury leading to tubulointerstitial fibrosis. However, current evidence on the mechanisms of progression of chronic kidney disease indicates that a complex interplay between glomeruli and tubules underlies progressive kidney injury. Primary glomerular injury can clearly lead to subsequent tubule injury. For example, damage to the glomerular filtration barrier can expose tubular cells to serum proteins, including complement and cytokines, that would not be present in physiological conditions and can promote the development of tubulointerstitial fibrosis and progressive decline in kidney function. In addition, although less well-studied, increasing evidence suggests that tubule injury, whether primary or secondary, can also promote glomerular damage. This feedback from the tubule to the glomerulus might be mediated by changes in the reabsorptive capacity of the tubule, which can affect the glomerular filtration rate, or by mediators released by injured proximal tubular cells that can induce damage in both podocytes and parietal epithelial cells. Examining the crosstalk between the various compartments of the kidney is important for understanding the mechanisms underlying kidney pathology and identifying potential therapeutic interventions. Glomerular injury and damage to the glomerular filtration barrier can promote the development of tubulointerstitial fibrosis. Here, the authors discuss potential mechanisms underlying this effect, as well as the emerging evidence of the tubule–glomerulus crosstalk that promotes glomerular damage following tubular injury.
{"title":"Crosstalk between glomeruli and tubules","authors":"Agnes B. Fogo, Raymond C. Harris","doi":"10.1038/s41581-024-00907-0","DOIUrl":"10.1038/s41581-024-00907-0","url":null,"abstract":"Models of kidney injury have classically concentrated on glomeruli as the primary site of injury leading to glomerulosclerosis or on tubules as the primary site of injury leading to tubulointerstitial fibrosis. However, current evidence on the mechanisms of progression of chronic kidney disease indicates that a complex interplay between glomeruli and tubules underlies progressive kidney injury. Primary glomerular injury can clearly lead to subsequent tubule injury. For example, damage to the glomerular filtration barrier can expose tubular cells to serum proteins, including complement and cytokines, that would not be present in physiological conditions and can promote the development of tubulointerstitial fibrosis and progressive decline in kidney function. In addition, although less well-studied, increasing evidence suggests that tubule injury, whether primary or secondary, can also promote glomerular damage. This feedback from the tubule to the glomerulus might be mediated by changes in the reabsorptive capacity of the tubule, which can affect the glomerular filtration rate, or by mediators released by injured proximal tubular cells that can induce damage in both podocytes and parietal epithelial cells. Examining the crosstalk between the various compartments of the kidney is important for understanding the mechanisms underlying kidney pathology and identifying potential therapeutic interventions. Glomerular injury and damage to the glomerular filtration barrier can promote the development of tubulointerstitial fibrosis. Here, the authors discuss potential mechanisms underlying this effect, as well as the emerging evidence of the tubule–glomerulus crosstalk that promotes glomerular damage following tubular injury.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 3","pages":"189-199"},"PeriodicalIF":28.6,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-06DOI: 10.1038/s41581-024-00906-1
Fabian Bock, Shensen Li, Ambra Pozzi, Roy Zent
The development and proper functioning of the kidney is dependent on the interaction of kidney cells with the surrounding extracellular matrix (ECM). These interactions are mediated by heterodimeric membrane-bound receptors called integrins, which bind to the ECM via their extracellular domain and via their cytoplasmic tail to intracellular adaptor proteins, to assemble large macromolecular adhesion complexes. These interactions enable integrins to control cellular functions such as intracellular signalling and organization of the actin cytoskeleton and are therefore crucial to organ function. The different nephron segments and the collecting duct system have unique morphologies, functions and ECM environments and are thus equipped with unique sets of integrins with distinct specificities for the ECM with which they interact. These cell-type-specific functions are facilitated by specific intracellular integrin binding proteins, which are critical in determining the integrin activation status, ligand-binding affinity and the type of ECM signals that are relayed to the intracellular structures. The spatiotemporal expression of integrins and their specific interactions with binding partners underlie the proper development, function and repair processes of the kidney. This Review summarizes our current understanding of how integrins, their binding partners and the actin cytoskeleton regulate kidney development, physiology and pathology. Integrins are heterodimeric transmembrane receptors that mediate crucial interactions between cells and extracellular matrix to regulate cellular functions such as intracellular signalling and organization of the actin cytoskeleton. This Review highlights the roles of integrins and integrin-binding proteins in the control of kidney-cell morphology and functions as well as their role in kidney diseases
{"title":"Integrins in the kidney — beyond the matrix","authors":"Fabian Bock, Shensen Li, Ambra Pozzi, Roy Zent","doi":"10.1038/s41581-024-00906-1","DOIUrl":"10.1038/s41581-024-00906-1","url":null,"abstract":"The development and proper functioning of the kidney is dependent on the interaction of kidney cells with the surrounding extracellular matrix (ECM). These interactions are mediated by heterodimeric membrane-bound receptors called integrins, which bind to the ECM via their extracellular domain and via their cytoplasmic tail to intracellular adaptor proteins, to assemble large macromolecular adhesion complexes. These interactions enable integrins to control cellular functions such as intracellular signalling and organization of the actin cytoskeleton and are therefore crucial to organ function. The different nephron segments and the collecting duct system have unique morphologies, functions and ECM environments and are thus equipped with unique sets of integrins with distinct specificities for the ECM with which they interact. These cell-type-specific functions are facilitated by specific intracellular integrin binding proteins, which are critical in determining the integrin activation status, ligand-binding affinity and the type of ECM signals that are relayed to the intracellular structures. The spatiotemporal expression of integrins and their specific interactions with binding partners underlie the proper development, function and repair processes of the kidney. This Review summarizes our current understanding of how integrins, their binding partners and the actin cytoskeleton regulate kidney development, physiology and pathology. Integrins are heterodimeric transmembrane receptors that mediate crucial interactions between cells and extracellular matrix to regulate cellular functions such as intracellular signalling and organization of the actin cytoskeleton. This Review highlights the roles of integrins and integrin-binding proteins in the control of kidney-cell morphology and functions as well as their role in kidney diseases","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 3","pages":"157-174"},"PeriodicalIF":28.6,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-06DOI: 10.1038/s41581-024-00908-z
J. David Smeijer, Donald E. Kohan, Neeraj Dhaun, Irene L. Noronha, Adrian Liew, Hiddo J. L. Heerspink
Endothelin-1 is a potent vasoconstrictor that has diverse physiological functions in the kidney, including in the regulation of blood flow and glomerular filtration, electrolyte homeostasis and endothelial function. Overexpression of endothelin-1 contributes to the pathophysiology of both diabetic and non-diabetic chronic kidney disease (CKD). Selective endothelin receptor antagonists (ERAs) that target the endothelin A (ETA) receptor have demonstrated benefits in animal models of kidney disease and in clinical trials. In patients with type 2 diabetes and CKD, the selective ETA ERA, atrasentan, reduced albuminuria and kidney function decline. Concerns about the increased risks of fluid retention and heart failure with ERA use have led to the design of further trials to optimize dosing and patient selection. More recent studies have shown that the dual ETA receptor and angiotensin receptor blocker, sparsentan, preserved kidney function with minimal fluid retention in patients with IgA nephropathy. Moreover, combined administration of a low dose of the ETA-selective ERA, zibotentan, with the sodium–glucose cotransporter 2 (SGLT2) inhibitor, dapagliflozin, enhanced albuminuria reduction and mitigated fluid retention in patients with CKD. Notably, sparsentan and aprocitentan have received FDA approval for the treatment of IgA nephropathy and treatment-resistant hypertension, respectively. This Review describes our current understanding of the use of ERAs in patients with CKD to guide their optimal safe and effective use in clinical practice. Endothelin-1 (ET-1) is a potent vasoactive peptide that is produced by various cell types of the kidney and regulates a variety of physiological processes. This Review describes the role of ET-1 in the kidney and in the development of chronic kidney disease, and the kidney-protective effects of endothelin-receptor antagonists in preclinical and clinical studies.
{"title":"Endothelin receptor antagonists in chronic kidney disease","authors":"J. David Smeijer, Donald E. Kohan, Neeraj Dhaun, Irene L. Noronha, Adrian Liew, Hiddo J. L. Heerspink","doi":"10.1038/s41581-024-00908-z","DOIUrl":"10.1038/s41581-024-00908-z","url":null,"abstract":"Endothelin-1 is a potent vasoconstrictor that has diverse physiological functions in the kidney, including in the regulation of blood flow and glomerular filtration, electrolyte homeostasis and endothelial function. Overexpression of endothelin-1 contributes to the pathophysiology of both diabetic and non-diabetic chronic kidney disease (CKD). Selective endothelin receptor antagonists (ERAs) that target the endothelin A (ETA) receptor have demonstrated benefits in animal models of kidney disease and in clinical trials. In patients with type 2 diabetes and CKD, the selective ETA ERA, atrasentan, reduced albuminuria and kidney function decline. Concerns about the increased risks of fluid retention and heart failure with ERA use have led to the design of further trials to optimize dosing and patient selection. More recent studies have shown that the dual ETA receptor and angiotensin receptor blocker, sparsentan, preserved kidney function with minimal fluid retention in patients with IgA nephropathy. Moreover, combined administration of a low dose of the ETA-selective ERA, zibotentan, with the sodium–glucose cotransporter 2 (SGLT2) inhibitor, dapagliflozin, enhanced albuminuria reduction and mitigated fluid retention in patients with CKD. Notably, sparsentan and aprocitentan have received FDA approval for the treatment of IgA nephropathy and treatment-resistant hypertension, respectively. This Review describes our current understanding of the use of ERAs in patients with CKD to guide their optimal safe and effective use in clinical practice. Endothelin-1 (ET-1) is a potent vasoactive peptide that is produced by various cell types of the kidney and regulates a variety of physiological processes. This Review describes the role of ET-1 in the kidney and in the development of chronic kidney disease, and the kidney-protective effects of endothelin-receptor antagonists in preclinical and clinical studies.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 3","pages":"175-188"},"PeriodicalIF":28.6,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-28DOI: 10.1038/s41581-024-00911-4
Chirag Raparia, Anne Davidson
New studies have revealed a novel homeostatic clearance function for medullary macrophages, unveiled roles for innate lymphoid cells and epithelial cells in orchestrating inflammation and fibrosis, and shown that clonal haematopoiesis influences the magnitude of inflammation in response to injury. These discoveries suggest therapeutic strategies to prevent kidney dysfunction associated with ageing and injury.
{"title":"Immune–stromal interplay shapes kidney function in health and disease","authors":"Chirag Raparia, Anne Davidson","doi":"10.1038/s41581-024-00911-4","DOIUrl":"10.1038/s41581-024-00911-4","url":null,"abstract":"New studies have revealed a novel homeostatic clearance function for medullary macrophages, unveiled roles for innate lymphoid cells and epithelial cells in orchestrating inflammation and fibrosis, and shown that clonal haematopoiesis influences the magnitude of inflammation in response to injury. These discoveries suggest therapeutic strategies to prevent kidney dysfunction associated with ageing and injury.","PeriodicalId":19059,"journal":{"name":"Nature Reviews Nephrology","volume":"21 2","pages":"71-72"},"PeriodicalIF":28.6,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142735725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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