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  1. Article ; Online: Role of perivascular cells in kidney homeostasis, inflammation, repair and fibrosis.

    Tanaka, Shinji / Portilla, Didier / Okusa, Mark D

    Nature reviews. Nephrology

    2023  Volume 19, Issue 11, Page(s) 721–732

    Abstract: Perivascular niches in the kidney comprise heterogeneous cell populations, including pericytes and fibroblasts, with distinct functions. These perivascular cells have crucial roles in preserving kidney homeostasis as they maintain microvascular networks ... ...

    Abstract Perivascular niches in the kidney comprise heterogeneous cell populations, including pericytes and fibroblasts, with distinct functions. These perivascular cells have crucial roles in preserving kidney homeostasis as they maintain microvascular networks by stabilizing the vasculature and regulating capillary constriction. A subset of kidney perivascular cells can also produce and secrete erythropoietin; this ability can be enhanced with hypoxia-inducible factor-prolyl hydroxylase inhibitors, which are used to treat anaemia in chronic kidney disease. In the pathophysiological state, kidney perivascular cells contribute to the progression of kidney fibrosis, partly via transdifferentiation into myofibroblasts. Moreover, perivascular cells are now recognized as major innate immune sentinels in the kidney that produce pro-inflammatory cytokines and chemokines following injury. These mediators promote immune cell infiltration, leading to persistent inflammation and progression of kidney fibrosis. The crosstalk between perivascular cells and tubular epithelial, immune and endothelial cells is therefore a key process in physiological and pathophysiological states. Here, we examine the multiple roles of kidney perivascular cells in health and disease, focusing on the latest advances in this field of research.
    MeSH term(s) Humans ; Pericytes ; Endothelial Cells/pathology ; Kidney/pathology ; Renal Insufficiency, Chronic/pathology ; Inflammation/pathology ; Fibrosis
    Language English
    Publishing date 2023-08-22
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-023-00752-7
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  2. Article ; Online: Role of intracellular complement activation in kidney fibrosis.

    Portilla, Didier / Xavier, Sandhya

    British journal of pharmacology

    2021  Volume 178, Issue 14, Page(s) 2880–2891

    Abstract: Increased expression of complement C1r, C1s and C3 in kidney cells plays an important role in the pathogenesis of kidney fibrosis. Our studies suggest that activation of complement in kidney cells with increased generation of C3 and its fragments occurs ... ...

    Abstract Increased expression of complement C1r, C1s and C3 in kidney cells plays an important role in the pathogenesis of kidney fibrosis. Our studies suggest that activation of complement in kidney cells with increased generation of C3 and its fragments occurs by activation of classical and alternative pathways. Single nuclei RNA sequencing studies in kidney tissue from unilateral ureteral obstruction mice show that increased synthesis of complement C3 and C5 occurs primarily in renal tubular epithelial cells (proximal and distal), while increased expression of complement receptors C3ar1 and C5ar1 occurs in interstitial cells including immune cells like monocytes/macrophages suggesting compartmentalization of complement components during kidney injury. Although global deletion of C3 and macrophage ablation prevent inflammation and reduced kidney tissue scarring, the development of mice with cell-specific deletion of complement components and their regulators could bring further insights into the mechanisms by which intracellular complement activation leads to fibrosis and progressive kidney disease. LINKED ARTICLES: This article is part of a themed issue on Canonical and non-canonical functions of the complement system in health and disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.14/issuetoc.
    MeSH term(s) Animals ; Complement Activation ; Fibrosis ; Kidney ; Kidney Diseases ; Macrophages ; Mice
    Language English
    Publishing date 2021-02-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.15408
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  3. Article ; Online: Apoptosis, fibrosis and senescence.

    Portilla, Didier

    Nephron. Clinical practice

    2014  Volume 127, Issue 1-4, Page(s) 65–69

    Abstract: Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form ... ...

    Abstract Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form of apoptosis or senescence. Recent studies have identified TWEAK, a tumor necrosis factor-like weak inducer of apoptosis, as a novel cytokine that mediates kidney inflammation in models of renal fibrosis. Inhibition of apoptosis via TWEAK inhibition has been shown to reduce kidney fibrosis. Recent studies using lineage tracing suggest that interstitial pericytes/perivascular fibroblasts differentiate into myofibroblasts and undergo proliferative expansion during fibrosis. Furthermore, increased expression of nuclear peroxisome proliferator-activated receptor-α in proximal tubules can directly reduce increased expression of transforming growth factor-β1 and interstitial inflammation in models of renal fibrosis, which suggests preservation of proximal tubule cell metabolism and integrity represents an important new therapeutic target. In this review, the current evidence and potential molecular mechanisms involved in the development of kidney fibrosis are discussed.
    MeSH term(s) Acute Kidney Injury/chemically induced ; Acute Kidney Injury/pathology ; Acute Kidney Injury/therapy ; Adenosine Triphosphate/metabolism ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins/antagonists & inhibitors ; Apoptosis Regulatory Proteins/physiology ; Cellular Senescence ; Cisplatin/toxicity ; Cytokine TWEAK ; Disease Progression ; Epithelial Cells/pathology ; Fatty Acids/metabolism ; Fibroblasts/pathology ; Fibrosis ; Gene Expression Profiling ; Humans ; Inflammation ; Kidney/pathology ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/pathology ; Mice ; Mice, Transgenic ; Molecular Targeted Therapy ; Myofibroblasts/pathology ; PPAR alpha/genetics ; PPAR alpha/metabolism ; PPAR alpha/physiology ; Pericytes/pathology ; Receptors, Tumor Necrosis Factor/physiology ; Renal Replacement Therapy ; TWEAK Receptor ; Tumor Necrosis Factors/physiology
    Chemical Substances Apoptosis Regulatory Proteins ; Cytokine TWEAK ; Fatty Acids ; PPAR alpha ; Receptors, Tumor Necrosis Factor ; TNFSF12 protein, human ; TWEAK Receptor ; Tnfsf12 protein, mouse ; Tumor Necrosis Factors ; Adenosine Triphosphate (8L70Q75FXE) ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2014-09-24
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 207121-6
    ISSN 1660-2110 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
    ISSN (online) 1660-2110 ; 1423-0186 ; 2235-3186
    ISSN 1660-8151 ; 0028-2766
    DOI 10.1159/000363717
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  4. Article: Apoptosis, Fibrosis and Senescence

    Portilla, Didier

    Nephron Clinical Practice

    2014  Volume 127, Issue 1-4, Page(s) 65–69

    Abstract: Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form ... ...

    Institution Division of Nephrology, Department of Internal Medicine, University of Virginia, Charlottesville, Va., and Salem Veterans Administration Medical Center, Salem, Va., USA
    Abstract Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form of apoptosis or senescence. Recent studies have identified TWEAK, a tumor necrosis factor-like weak inducer of apoptosis, as a novel cytokine that mediates kidney inflammation in models of renal fibrosis. Inhibition of apoptosis via TWEAK inhibition has been shown to reduce kidney fibrosis. Recent studies using lineage tracing suggest that interstitial pericytes/perivascular fibroblasts differentiate into myofibroblasts and undergo proliferative expansion during fibrosis. Furthermore, increased expression of nuclear peroxisome proliferator-activated receptor-α in proximal tubules can directly reduce increased expression of transforming growth factor-β1 and interstitial inflammation in models of renal fibrosis, which suggests preservation of proximal tubule cell metabolism and integrity represents an important new therapeutic target. In this review, the current evidence and potential molecular mechanisms involved in the development of kidney fibrosis are discussed.
    Keywords Acute kidney injury ; Apoptosis ; Cellular senescence ; Epithelial cell injury ; Fibrosis ; Proximal tubule metabolism
    Language English
    Publishing date 2014-09-24
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Original Paper
    ZDB-ID 207121-6
    ISSN 1660-2110 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
    ISSN (online) 1660-2110 ; 1423-0186 ; 2235-3186
    ISSN 1660-8151 ; 0028-2766
    DOI 10.1159/000363717
    Database Karger publisher's database

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  5. Article ; Online: Apoptosis, Fibrosis and Senescence

    Portilla, Didier

    Nephron Clinical Practice

    2014  Volume 127, Issue 1-4, Page(s) 65–69

    Abstract: Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form ... ...

    Abstract Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form of apoptosis or senescence. Recent studies have identified TWEAK, a tumor necrosis factor-like weak inducer of apoptosis, as a novel cytokine that mediates kidney inflammation in models of renal fibrosis. Inhibition of apoptosis via TWEAK inhibition has been shown to reduce kidney fibrosis. Recent studies using lineage tracing suggest that interstitial pericytes/perivascular fibroblasts differentiate into myofibroblasts and undergo proliferative expansion during fibrosis. Furthermore, increased expression of nuclear peroxisome proliferator-activated receptor-α in proximal tubules can directly reduce increased expression of transforming growth factor-β1 and interstitial inflammation in models of renal fibrosis, which suggests preservation of proximal tubule cell metabolism and integrity represents an important new therapeutic target. In this review, the current evidence and potential molecular mechanisms involved in the development of kidney fibrosis are discussed.© 2014 S. Karger AG, Basel
    Keywords Acute kidney injury ; Apoptosis ; Cellular senescence ; Epithelial cell injury ; Fibrosis ; Proximal tubule metabolism
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 207121-6
    ISSN 1660-2110 ; 1423-0186 ; 0028-2766 ; 1660-2110 ; 0028-2766
    ISSN (online) 1660-2110 ; 1423-0186
    ISSN 1660-2110 ; 0028-2766
    DOI 10.1159/000363717
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  6. Article ; Online: Serum metabolite profiles predict outcomes in critically ill patients receiving renal replacement therapy.

    Sun, Jinchun / Cao, Zhijun / Schnackenberg, Laura / Pence, Lisa / Yu, Li-Rong / Choudhury, Devasmita / Palevsky, Paul M / Portilla, Didier / Beger, Richard D

    Journal of chromatography. B, Analytical technologies in the biomedical and life sciences

    2021  Volume 1187, Page(s) 123024

    Abstract: Acute kidney injury (AKI) requiring renal replacement therapy (RRT) is associated with increased incidence of dialysis dependence and portends high mortality in critically ill patients. At the early stage of RRT, serum metabolic biomarkers might ... ...

    Abstract Acute kidney injury (AKI) requiring renal replacement therapy (RRT) is associated with increased incidence of dialysis dependence and portends high mortality in critically ill patients. At the early stage of RRT, serum metabolic biomarkers might differntiate patients with a high risk of mortality or permanent kidney injury from those who can recover. Serum samples from participants enrolled in the Veteran's Affairs/National Institutes of Health Acute Renal Failure Trial Network study were collected on day 1 (n = 97) and day 8 (n = 105) of randomized RRT. The samples were further evaluated using LC/MS-based metabolic profiling. A model predicting mortality by day 8 was built from samples collected on day 1 and based on four metabolites with an area under the curve (AUC) of 0.641. A model most predictive of mortality by day 28 was built from the levels of 11 serum metabolites from day 8 with an AUC of 0.789. Both day 1 and day 8 samples had lower serum levels of 1-arachidonoyl-lysoPC and 1-eicosatetraenoyl-lysoPC (involved in anti-inflammatory processes) in the critically ill patients who died by day 8 or day 28. Higher levels of amino acids and amino acid metabolites in the day 8 model predicting < day 28 mortality may be indicative of muscle wasting. A kidney recovery biomarker panel based on the serum levels of three metabolites from day 8 samples with an AUC of 0.70 was devised. Serum metabolic profiling of AKI critically ill patients requiring RRT revealed predictive models of mortality based on observed differences in four serum metabolites at day 1 and 11 metabolites at day 8 which were predictive of mortality. Significant changes in the levels of these metabolites suggest links to inflammatory processes and/or muscle wasting.
    MeSH term(s) Acute Kidney Injury/blood ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/mortality ; Acute Kidney Injury/therapy ; Adult ; Aged ; Biomarkers/blood ; Biomarkers/metabolism ; Cohort Studies ; Critical Illness ; Female ; Humans ; Male ; Metabolome/physiology ; Metabolomics ; Middle Aged ; Models, Statistical ; Renal Replacement Therapy
    Chemical Substances Biomarkers
    Language English
    Publishing date 2021-11-06
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1180823-8
    ISSN 1873-376X ; 0378-4347 ; 1570-0232 ; 1387-2273
    ISSN (online) 1873-376X
    ISSN 0378-4347 ; 1570-0232 ; 1387-2273
    DOI 10.1016/j.jchromb.2021.123024
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  7. Article ; Online: Biomarkers of Transplant Tolerance: A Provisional Analysis for an Unmet Need.

    Mas, Valeria R / Portilla, Didier / Maluf, Daniel G

    Transplantation

    2016  Volume 100, Issue 4, Page(s) 705–706

    MeSH term(s) Animals ; Graft Rejection/metabolism ; Graft Survival ; Liver/surgery ; Liver Transplantation ; Male ; MicroRNAs/metabolism ; Transplantation Tolerance
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2016-04
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 208424-7
    ISSN 1534-6080 ; 0041-1337
    ISSN (online) 1534-6080
    ISSN 0041-1337
    DOI 10.1097/TP.0000000000001106
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  8. Article: Energy metabolism and cytotoxicity.

    Portilla, Didier

    Seminars in nephrology

    2003  Volume 23, Issue 5, Page(s) 432–438

    Abstract: Fatty acids constitute a major source of metabolic fuel for energy production in kidney tissue. During acute renal failure (ARF) injury to the proximal tubule and medullary thick ascending limb leads to structural and functional alterations that result ... ...

    Abstract Fatty acids constitute a major source of metabolic fuel for energy production in kidney tissue. During acute renal failure (ARF) injury to the proximal tubule and medullary thick ascending limb leads to structural and functional alterations that result in reduced expression and activity of mitochondrial and peroxisomal fatty acid oxidation (FAO) enzymes. Reduced DNA binding activity of peroxisome proliferator activated receptor-alpha (PPARalpha) to its target genes and decreased expression of its tissue-specific coactivator PPAR-gamma-coactivator-1 (PGC-1) in the mouse proximal tubule and the medullary thick ascending limb, represent 2 potential mechanisms that account for the observed alterations of FAO during ARF. Pretreatment with PPARalpha ligands restores the expression and activity of renal FAO enzymes, and this metabolic alteration leads to amelioration of acute tubular necrosis caused by ischemia/reperfusion or cisplatin-induced ARF. More studies are needed to examine further the cellular mechanisms of substrate inhibition, and to determine if metabolic pathways, in addition to the recovery of FAO, account for the protective effect (s) of PPARalpha ligands during acute renal failure.
    MeSH term(s) Acute Kidney Injury/metabolism ; Cell Death/physiology ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Fatty Acids/metabolism ; Gene Expression Regulation/physiology ; Humans ; Mitochondria/metabolism ; Oxidation-Reduction ; Peroxisomes/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Transcription Factors/metabolism
    Chemical Substances Fatty Acids ; Receptors, Cytoplasmic and Nuclear ; Transcription Factors
    Language English
    Publishing date 2003-10-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604652-6
    ISSN 1558-4488 ; 0270-9295
    ISSN (online) 1558-4488
    ISSN 0270-9295
    DOI 10.1016/s0270-9295(03)00088-3
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  9. Article: Serum metabolite profiles predict outcomes in critically ill patients receiving renal replacement therapy

    Sun, Jinchun / Cao, Zhijun / Schnackenberg, Laura / Pence, Lisa / Yu, Li-Rong / Choudhury, Devasmita / Palevsky, Paul M. / Portilla, Didier / Beger, Richard D.

    Journal of chromatography. 2021 Dec. 15, v. 1187

    2021  

    Abstract: Acute kidney injury (AKI) requiring renal replacement therapy (RRT) is associated with increased incidence of dialysis dependence and portends high mortality in critically ill patients. At the early stage of RRT, serum metabolic biomarkers might ... ...

    Abstract Acute kidney injury (AKI) requiring renal replacement therapy (RRT) is associated with increased incidence of dialysis dependence and portends high mortality in critically ill patients. At the early stage of RRT, serum metabolic biomarkers might differntiate patients with a high risk of mortality or permanent kidney injury from those who can recover. Serum samples from participants enrolled in the Veteran’s Affairs/National Institutes of Health Acute Renal Failure Trial Network study were collected on day 1 (n = 97) and day 8 (n = 105) of randomized RRT. The samples were further evaluated using LC/MS-based metabolic profiling. A model predicting mortality by day 8 was built from samples collected on day 1 and based on four metabolites with an area under the curve (AUC) of 0.641. A model most predictive of mortality by day 28 was built from the levels of 11 serum metabolites from day 8 with an AUC of 0.789. Both day 1 and day 8 samples had lower serum levels of 1-arachidonoyl-lysoPC and 1-eicosatetraenoyl-lysoPC (involved in anti-inflammatory processes) in the critically ill patients who died by day 8 or day 28. Higher levels of amino acids and amino acid metabolites in the day 8 model predicting < day 28 mortality may be indicative of muscle wasting. A kidney recovery biomarker panel based on the serum levels of three metabolites from day 8 samples with an AUC of 0.70 was devised. Serum metabolic profiling of AKI critically ill patients requiring RRT revealed predictive models of mortality based on observed differences in four serum metabolites at day 1 and 11 metabolites at day 8 which were predictive of mortality. Significant changes in the levels of these metabolites suggest links to inflammatory processes and/or muscle wasting.
    Keywords acute kidney injury ; amino acids ; biomarkers ; blood serum ; chromatography ; dialysis ; hemodialysis ; kidneys ; metabolites ; models ; mortality ; muscles ; risk
    Language English
    Dates of publication 2021-1215
    Publishing place Elsevier B.V.
    Document type Article
    ISSN 1570-0232
    DOI 10.1016/j.jchromb.2021.123024
    Database NAL-Catalogue (AGRICOLA)

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  10. Article ; Online: Folic acid-mediated fibrosis is driven by C5a receptor 1-mediated activation of kidney myeloid cells.

    Sahu, Ranjit K / Xavier, Sandhya / Chauss, Daniel / Wang, Luopin / Chew, Claude / Taylor, Ronald / Stallcup, William B / Ma, Jennie Z / Kazemian, Majid / Afzali, Behdad / Köhl, Jörg / Portilla, Didier

    American journal of physiology. Renal physiology

    2022  Volume 322, Issue 6, Page(s) F597–F610

    Abstract: We have previously reported that increased expression and activation of kidney cell complement components play an important role in the pathogenesis of renal scarring. Here, we used floxed green fluorescent protein (GFP)-C5a receptor 1 (C5aR1) knockin ... ...

    Abstract We have previously reported that increased expression and activation of kidney cell complement components play an important role in the pathogenesis of renal scarring. Here, we used floxed green fluorescent protein (GFP)-C5a receptor 1 (C5aR1) knockin mice (GFP-
    MeSH term(s) Animals ; Cicatrix ; Fibrosis ; Folic Acid/pharmacology ; Green Fluorescent Proteins ; Kidney/pathology ; Mice ; Mice, Knockout ; Myeloid Cells/pathology ; Receptor, Anaphylatoxin C5a/genetics ; Receptors, Platelet-Derived Growth Factor
    Chemical Substances Receptor, Anaphylatoxin C5a ; Green Fluorescent Proteins (147336-22-9) ; Folic Acid (935E97BOY8) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2022-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00404.2021
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