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Article ; Online: Cellular and molecular mechanisms of renal fibrosis.

Liu, Youhua

2011 Volume 7, Issue 12, Page(s) 684–696

Abstract: ... our current understanding of the cellular and molecular mechanisms of renal fibrosis, which could offer novel ... all progressive chronic kidney diseases. Renal fibrosis is also a reliable predictor of prognosis and a major ... Multiple cellular and molecular events, such as tubular atrophy, microvascular rarefaction and tissue hypoxia ...

Abstract	Renal fibrosis, particularly tubulointerstitial fibrosis, is the common final outcome of almost all progressive chronic kidney diseases. Renal fibrosis is also a reliable predictor of prognosis and a major determinant of renal insufficiency. Irrespective of the initial causes, renal fibrogenesis is a dynamic and converging process that consists of four overlapping phases: priming, activation, execution and progression. Nonresolving inflammation after a sustained injury sets up the fibrogenic stage (priming) and triggers the activation and expansion of matrix-producing cells from multiple sources through diverse mechanisms, including activation of interstitial fibroblasts and pericytes, phenotypic conversion of tubular epithelial and endothelial cells and recruitment of circulating fibrocytes. Upon activation, matrix-producing cells assemble a multicomponent, integrin-associated protein complex that integrates input from various fibrogenic signals and orchestrates the production of matrix components and their extracellular assembly. Multiple cellular and molecular events, such as tubular atrophy, microvascular rarefaction and tissue hypoxia, promote scar formation and ensure a vicious progression to end-stage kidney failure. This Review outlines our current understanding of the cellular and molecular mechanisms of renal fibrosis, which could offer novel insights into the development of new therapeutic strategies.
MeSH term(s)	Disease Progression ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/pathology ; Fibrosis ; Humans ; Kidney/metabolism ; Kidney/pathology ; Kidney Diseases/metabolism ; Kidney Diseases/pathology
Chemical Substances	Extracellular Matrix Proteins
Language	English
Publishing date	2011-10-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2011.149
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Article ; Online: Cellular and Molecular Mechanisms of Intestinal Fibrosis.

Wu, Xiaomin / Lin, Xiaoxuan / Tan, Jinyu / Liu, Zishan / He, Jinshen / Hu, Fan / Wang, Yu / Chen, Minhu / Liu, Fen / Mao, Ren

Gut and liver

2023 Volume 17, Issue 3, Page(s) 360–374

Abstract: ... made in elucidating the cellular and molecular mechanisms of intestinal fibrosis. Here, we summarized ... new discoveries and advances of cellular components and major molecular mediators that are associated ... Several inflammation-independent mechanisms including gut microbiota, creeping fat, ECM interaction, and metabolic ...

Abstract	Intestinal fibrosis associated stricture is a common complication of inflammatory bowel disease usually requiring endoscopic or surgical intervention. Effective anti-fibrotic agents aiming to control or reverse intestinal fibrosis are still unavailable. Thus, clarifying the mechanism underpinning intestinal fibrosis is imperative. Fibrosis is characterized by an excessive accumulation of extracellular matrix (ECM) proteins at the injured sites. Multiple cellular types are implicated in fibrosis development. Among these cells, mesenchymal cells are major compartments that are activated and then enhance the production of ECM. Additionally, immune cells contribute to the persistent activation of mesenchymal cells and perpetuation of inflammation. Molecules are messengers of crosstalk between these cellular compartments. Although inflammation is necessary for fibrosis development, purely controlling intestinal inflammation cannot halt the development of fibrosis, suggesting that chronic inflammation is not the unique contributor to fibrogenesis. Several inflammation-independent mechanisms including gut microbiota, creeping fat, ECM interaction, and metabolic reprogramming are involved in the pathogenesis of fibrosis. In the past decades, substantial progress has been made in elucidating the cellular and molecular mechanisms of intestinal fibrosis. Here, we summarized new discoveries and advances of cellular components and major molecular mediators that are associated with intestinal fibrosis, aiming to provide a basis for exploring effective anti-fibrotic therapies in this field.
MeSH term(s)	Humans ; Intestines/pathology ; Inflammatory Bowel Diseases ; Fibrosis ; Inflammation
Language	English
Publishing date	2023-03-10
Publishing country	Korea (South)
Document type	Journal Article ; Review ; Comment
ZDB-ID	2399010-7
ISSN	2005-1212 ; 1976-2283
ISSN (online)	2005-1212
ISSN	1976-2283
DOI	10.5009/gnl220045
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Article ; Online: Cellular and Molecular Pathways Underlying the Nephrotoxicity of Gadolinium.

Reis Sousa, Nícia / Rocha, Susana / Santos-Silva, Alice / Coimbra, Susana / Valente, Maria João

Toxicological sciences : an official journal of the Society of Toxicology

2022 Volume 186, Issue 1, Page(s) 134–148

Abstract: ... of these agents. This study aimed at unveiling the cellular and molecular mechanisms of nephrotoxicity of Gd (III ... disease, including inflammation, hypoxia, and fibrosis. Our results give new insights into the mechanisms ... the expression of modulators of various signaling pathways involved in the development and progression of renal ...

Abstract	Mounting evidence on the short- and long-term adverse effects associated with gadolinium [Gd (III)]-based contrast agents used in magnetic resonance imaging have emerged in the past 3 decades. Safety issues arise from the release of Gd (III) from chelates and its deposition in tissues, which is exacerbated in patients with renal disease, because the kidney is the major excretion organ of most of these agents. This study aimed at unveiling the cellular and molecular mechanisms of nephrotoxicity of Gd (III), using an in vitro model of human proximal tubular cells (HK-2 cell line). Cell viability declined in a concentration- and time-dependent manner after exposure to GdCl3·6H2O. The estimated inhibitory concentrations (ICs) eliciting 1%-50% of cell death, after 24 h of exposure, ranged from 3.4 to 340.5 µM. At toxic concentrations, exposure to Gd (III) led to disruption of the oxidative status, mitochondrial dysfunction, cell death by apoptosis, switching to necrosis at higher levels, and autophagic activation. Disturbance of the lipid metabolism was already observed at low-toxicity ICs, with accumulation of lipid droplets, and upregulation of genes related to both lipogenesis and lipolysis. Gd (III)-exposure, even at the subtoxic IC01, increased the expression of modulators of various signaling pathways involved in the development and progression of renal disease, including inflammation, hypoxia, and fibrosis. Our results give new insights into the mechanisms underlying the nephrotoxic potential of Gd (III) and highlight the need to further clarify the risks versus benefits of the Gd (III)-based contrast agents currently in use.
MeSH term(s)	Apoptosis ; Contrast Media/toxicity ; Gadolinium/toxicity ; Humans ; Magnetic Resonance Imaging ; Renal Insufficiency/chemically induced
Chemical Substances	Contrast Media ; Gadolinium (AU0V1LM3JT)
Language	English
Publishing date	2022-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfab148
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Article ; Online: The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms.

Liu, Jia / Wang, Faping / Luo, Fengming

Biomolecules

2023 Volume 13, Issue 1

Abstract: ... for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT ... of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has ... molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT ...

Abstract	There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between JAK/STAT and the pathophysiology of fibrotic diseases was noticed, including the liver, renal, heart, bone marrow, and lung. JAK inhibitor has been approved for myelofibrosis, and subsequently, JAK/STAT may serve as a promising target for fibrosis in other organs. Therefore, this article reviews the roles and mechanisms of the JAK/STAT signaling pathway in fibrotic diseases.
MeSH term(s)	Animals ; Humans ; Janus Kinases/metabolism ; Signal Transduction/physiology ; STAT Transcription Factors/genetics ; STAT Transcription Factors/metabolism ; Neoplasms/metabolism ; Fibrosis ; Mammals/metabolism
Chemical Substances	Janus Kinases (EC 2.7.10.2) ; STAT Transcription Factors
Language	English
Publishing date	2023-01-06
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13010119
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Article ; Online: Single-cell dissection of cellular and molecular features underlying mesenchymal stem cell therapy in ischemic acute kidney injury.

Wang, Wenjuan / Zhang, Min / Ren, Xuejing / Song, Yanqi / Xu, Yue / Zhuang, Kaiting / Xiao, Tuo / Guo, Xinru / Wang, Siyang / Hong, Quan / Feng, Zhe / Chen, Xiangmei / Cai, Guangyan

Molecular therapy : the journal of the American Society of Gene Therapy

2023 Volume 31, Issue 10, Page(s) 3067–3083

Abstract: ... renal fibrosis. Finally, in addition to activating the repair properties of renal progenitor/stem cells ... suggested that profibrotic TECs expressing pro-fibrotic factors such as Zeb2 and Pdgfb promoted ... the recruitment of inflammatory monocytes and Th17 cells to injured kidney tissue, inducing TGF-β1 secretion and ...

Abstract	Mesenchymal stem cells (MSCs) exert beneficial therapeutic effects in acute kidney injury (AKI), while the detailed repair mechanism remains unclear. Herein, we probed the underlying mechanisms of MSC therapy in AKI by performing unbiased single-cell RNA sequencing in IRI model with/without MSC treatment. Our analyses uncovered the tubular epithelial cells (TECs) and immune cells transcriptomic diversity and highlighted a repair trajectory involving renal stem/progenitor cell differentiation. Our findings also suggested that profibrotic TECs expressing pro-fibrotic factors such as Zeb2 and Pdgfb promoted the recruitment of inflammatory monocytes and Th17 cells to injured kidney tissue, inducing TGF-β1 secretion and renal fibrosis. Finally, in addition to activating the repair properties of renal progenitor/stem cells, we uncovered a role for MSC-derived miR-26a-5p in mediating the therapeutic effects of MSCs by inhibiting Zeb2 expression and suppressing pro-fibrotic TECs and its subsequent recruitment of immune cell subpopulations. These findings may help to optimize future AKI treatment strategies.
Language	English
Publishing date	2023-08-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2023.07.024
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Zs.A 5640: Show issues

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Article ; Online: Radiation-induced kidney toxicity: molecular and cellular pathogenesis.

Klaus, Richard / Niyazi, Maximilian / Lange-Sperandio, Bärbel

Radiation oncology (London, England)

2021 Volume 16, Issue 1, Page(s) 43

Abstract: ... The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation ... that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested ... of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress ...

Abstract	Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin-angiotensin-aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.
MeSH term(s)	Animals ; Cellular Senescence/radiation effects ; DNA Damage/radiation effects ; Fibrosis ; Humans ; Hypertension, Renovascular/diagnosis ; Hypertension, Renovascular/etiology ; Hypertension, Renovascular/pathology ; Hypertension, Renovascular/therapy ; Inflammation ; Kidney/injuries ; Kidney/pathology ; Kidney/radiation effects ; Oxidative Stress/radiation effects ; Radiation Injuries/diagnosis ; Radiation Injuries/etiology ; Radiation Injuries/pathology ; Radiation Injuries/therapy ; Radiotherapy/adverse effects ; Renin-Angiotensin System/radiation effects
Language	English
Publishing date	2021-02-25
Publishing country	England
Document type	Journal Article ; Review
ISSN	1748-717X
ISSN (online)	1748-717X
DOI	10.1186/s13014-021-01764-y
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Article ; Online: Cellular Senescence in Renal and Urinary Tract Disorders.

Santin, Yohan / Lluel, Philippe / Rischmann, Pascal / Gamé, Xavier / Mialet-Perez, Jeanne / Parini, Angelo

Cells

2020 Volume 9, Issue 11

Abstract: ... in renal, prostate, and bladder disorders. In this review, we will summarize the molecular mechanisms ... adverse remodeling, and fibrosis. Recently, an increase in senescent cell burden has been reported ... of senescence and their implication in renal and urinary tract diseases. We will also discuss the differential ...

Abstract	Cellular senescence is a state of cell cycle arrest induced by repetitive cell mitoses or different stresses, which is implicated in various physiological or pathological processes. The beneficial or adverse effects of senescent cells depend on their transitory or persistent state. Transient senescence has major beneficial roles promoting successful post-injury repair and inhibiting malignant transformation. On the other hand, persistent accumulation of senescent cells has been associated with chronic diseases and age-related illnesses like renal/urinary tract disorders. The deleterious effects of persistent senescent cells have been related, in part, to their senescence-associated secretory phenotype (SASP) characterized by the release of a variety of factors responsible for chronic inflammation, extracellular matrix adverse remodeling, and fibrosis. Recently, an increase in senescent cell burden has been reported in renal, prostate, and bladder disorders. In this review, we will summarize the molecular mechanisms of senescence and their implication in renal and urinary tract diseases. We will also discuss the differential impacts of transient versus persistent status of cellular senescence, as well as the therapeutic potential of senescent cell targeting in these diseases.
MeSH term(s)	Animals ; Cellular Senescence ; Humans ; Kidney Diseases/pathology ; Kidney Diseases/physiopathology ; Kidney Diseases/therapy ; Organ Specificity ; Signal Transduction ; Urologic Diseases/pathology ; Urologic Diseases/physiopathology ; Urologic Diseases/therapy
Language	English
Publishing date	2020-11-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9112420
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Article ; Online: Stanniocalcin‑1 suppresses TGF‑β‑induced mitochondrial dysfunction and cellular fibrosis in human renal proximal tubular cells.

Yang, Eun Mi / Park, Jung Sun / Joo, Soo Yeon / Bae, Eun Hui / Ma, Seong Kwon / Kim, Soo Wan

International journal of molecular medicine

2022 Volume 50, Issue 2

Abstract: ... the protective role of recombinant STC1 (rSTC1) in renal fibrosis and to identify the mechanisms underlying ... cellular fibrosis in HK2 human renal proximal tubular cells. Semi‑quantitative PCR, western blot analysis ... Treatment of HK2 cells with TGF‑β reduced the MMP and increased the production of reactive oxygen species ...

Abstract	Stanniocalcin‑1 (STC1), a multifunctional glycoprotein with antioxidant and anti‑inflammatory properties, serves an important role in kidney protection. STC1 is one of the few hormones targeted to the mitochondria to regulate mitochondrial quality control by suppressing oxidative stress and mitochondrial damage. However, the mechanisms underlying the effect of STC1 remain unclear. The present study aimed to investigate the protective role of recombinant STC1 (rSTC1) in renal fibrosis and to identify the mechanisms underlying cellular fibrosis in HK2 human renal proximal tubular cells. Semi‑quantitative PCR, western blot analysis and confocal microscopy were used to detect the mRNA levels, protein levels and mitochondrial membrane potential (MMP). Mitochondrial superoxide production was evaluated using MitoSox staining. rSTC1 attenuated TGF‑β‑induced downregulation of AMP‑activated protein kinase and uncoupling protein 2 (UCP2). Treatment of HK2 cells with TGF‑β reduced the MMP and increased the production of reactive oxygen species (ROS). In addition, TGF‑β treatment upregulated fibrotic markers, such as α‑SMA and fibronectin, in HK2 cells. Treatment with rSTC1 and TGF‑β suppressed mitochondrial ROS production by recovering the MMP and reversed the upregulation of fibrotic markers in HK2 cells. The effects of rSTC1 were reversed when UCP2 expression was silenced. The present study revealed a novel role of STC1 in preventing TGF‑β induced cellular fibrosis in HK2 cells.
MeSH term(s)	Fibrosis ; Glycoproteins/metabolism ; Humans ; Kidney/metabolism ; Matrix Metalloproteinases/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Transforming Growth Factor beta/metabolism ; Uncoupling Protein 2
Chemical Substances	Glycoproteins ; Reactive Oxygen Species ; Transforming Growth Factor beta ; Uncoupling Protein 2 ; teleocalcin (76687-96-2) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2022-06-22
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1444428-8
ISSN	1791-244X ; 1107-3756
ISSN (online)	1791-244X
ISSN	1107-3756
DOI	10.3892/ijmm.2022.5163
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Zs.A 4942: Show issues

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Article ; Online: Fibrotic Scar in CNS Injuries: From the Cellular Origins of Fibroblasts to the Molecular Processes of Fibrotic Scar Formation.

Ayazi, Maryam / Zivkovic, Sandra / Hammel, Grace / Stefanovic, Branko / Ren, Yi

Cells

2022 Volume 11, Issue 15

Abstract: ... regeneration. While discussing the shared features of CNS fibrotic scar and fibrosis outside the CNS ... formation in CNS trauma, including the cellular origins of fibroblasts, the mechanism of fibrotic scar ... formation following an injury, as well as the implication of the fibrotic scar in CNS tissue remodeling and ...

Abstract	Central nervous system (CNS) trauma activates a persistent repair response that leads to fibrotic scar formation within the lesion. This scarring is similar to other organ fibrosis in many ways; however, the unique features of the CNS differentiate it from other organs. In this review, we discuss fibrotic scar formation in CNS trauma, including the cellular origins of fibroblasts, the mechanism of fibrotic scar formation following an injury, as well as the implication of the fibrotic scar in CNS tissue remodeling and regeneration. While discussing the shared features of CNS fibrotic scar and fibrosis outside the CNS, we highlight their differences and discuss therapeutic targets that may enhance regeneration in the CNS.
MeSH term(s)	Central Nervous System/pathology ; Cicatrix/pathology ; Fibroblasts/pathology ; Fibrosis ; Humans ; Spinal Cord Injuries/pathology ; Trauma, Nervous System
Language	English
Publishing date	2022-08-02
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11152371
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Article ; Online: Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy.

Klinkhammer, Barbara Mara / Djudjaj, Sonja / Kunter, Uta / Palsson, Runolfur / Edvardsson, Vidar Orn / Wiech, Thorsten / Thorsteinsdottir, Margret / Hardarson, Sverrir / Foresto-Neto, Orestes / Mulay, Shrikant R / Moeller, Marcus Johannes / Jahnen-Dechent, Wilhelm / Floege, Jürgen / Anders, Hans-Joachim / Boor, Peter

Journal of the American Society of Nephrology : JASN

2020 Volume 31, Issue 4, Page(s) 799–816

Abstract: ... process that we term : Conclusions: Rodent models of the cellular and molecular mechanisms of 2,8-DHA ... by crystal deposits, tubular injury, inflammation, and fibrosis. Kidney injury depended on crystal size ... intake is unknown.: Methods: Using animal models and patient kidney biopsies, we assessed ...

Abstract	Background: Hereditary deficiency of adenine phosphoribosyltransferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation of 2,8-DHA crystals within renal tubules. Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unknown. Methods: Using animal models and patient kidney biopsies, we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage. We also used knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2-HS glycoprotein (AHSG), all of which are involved in the pathogenesis of other types of crystal-induced nephropathies. Results: Adenine-enriched diet in mice induced 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubular injury, inflammation, and fibrosis. Kidney injury depended on crystal size. The smallest crystals were endocytosed by tubular epithelial cells. Crystals of variable size were excreted in urine. Large crystals obstructed whole tubules. Medium-sized crystals induced a particular reparative process that we term Conclusions: Rodent models of the cellular and molecular mechanisms of 2,8-DHA nephropathy and crystal clearance have clinical relevance and offer insight into potential future targets for therapeutic interventions.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/physiology ; Adenine Phosphoribosyltransferase/deficiency ; Adenine Phosphoribosyltransferase/metabolism ; Adult ; Animals ; Cohort Studies ; Diet ; Disease Models, Animal ; Female ; Humans ; Infant ; Kidney Diseases/etiology ; Kidney Diseases/pathology ; Male ; Metabolism, Inborn Errors/etiology ; Metabolism, Inborn Errors/metabolism ; Metabolism, Inborn Errors/pathology ; Mice ; Middle Aged ; Urolithiasis/etiology ; Urolithiasis/metabolism ; Urolithiasis/pathology
Chemical Substances	2,8-dihydroxyadenine (30377-37-8) ; Adenine Phosphoribosyltransferase (EC 2.4.2.7) ; Adenine (JAC85A2161)
Language	English
Publishing date	2020-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2019080827
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