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Article ; Online: Ataxia Telangiectasia and Rad3-Related Activation by DNA Damage Mitigates Maladaptive Repair after Acute Kidney Injury.

Bonventre, Joseph V

2021 Volume 146, Issue 3, Page(s) 274–277

Abstract: DNA damage is an important consequence of injury to the proximal tubule. The proximal tubule cell responds to this damage by mounting a DNA damage response (DDR). Two protein kinases, ataxia-telangiectasia mutated (ATM) or ataxia telangiectasia and Rad3- ... ...

Abstract	DNA damage is an important consequence of injury to the proximal tubule. The proximal tubule cell responds to this damage by mounting a DNA damage response (DDR). Two protein kinases, ataxia-telangiectasia mutated (ATM) or ataxia telangiectasia and Rad3-related (ATR), play an important role in this DDR. If efficient, the DDR can lead to repair of the DNA, cell renewal, and return to a healthy state. In many cases, however, especially in the setting of baseline kidney injury, there is incomplete repair. In human chronic kidney disease (CKD) and in human kidney organoids exposed to acute injury, there is increased evidence of DNA damage and activation of ATR. This review focuses on 3 aspects of the DNA damage and response to it: (1) DNA damage and the DDR precipitated by acute injury; (2) protection afforded by the DDR kinase, ATR, in multiple mouse models of acute kidney injury; and (3) downstream effects of genetic inhibition of ATR in the proximal tubule, leading to maladaptive repair, fibrosis, and CKD.
MeSH term(s)	Acute Kidney Injury/genetics ; Animals ; Ataxia Telangiectasia ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; DNA Damage ; Female ; Humans ; Male ; Mice ; Renal Insufficiency, Chronic/genetics
Chemical Substances	Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1)
Language	English
Publishing date	2021-10-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000519447
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Book: Biomarkers

Vaidya, Vishal S. / Bonventre, Joseph V.

in medicine, drug discovery, and environmental health

2010

Author's details	ed. by Vishal S. Vaidya ; Joseph V. Bonventre
Keywords	Biological Markers ; Diagnostic Techniques and Procedures ; Drug Discovery ; Environmental Monitoring / methods
Language	English
Size	XXVIII, 602 S., [8] Bl. : Ill., graph. Darst.
Publisher	Wiley
Publishing place	Hoboken, NJ
Publishing country	United States
Document type	Book
HBZ-ID	HT016589631
ISBN	978-0-470-45224-0 ; 0-470-45224-2
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Article ; Online: Kidney organoids-a new tool for kidney therapeutic development.

Bonventre, Joseph V

Kidney international

2018 Volume 94, Issue 6, Page(s) 1040–1042

Abstract: Kidney organoids, derived from human pluripotent stem cells, have the potential to greatly facilitate drug development. Boreström et al. have used CRISPR/Cas9 to create kidney fluorescent lineage markers for SIX2 and NPHS1 to monitor the differentiation ... ...

Abstract	Kidney organoids, derived from human pluripotent stem cells, have the potential to greatly facilitate drug development. Boreström et al. have used CRISPR/Cas9 to create kidney fluorescent lineage markers for SIX2 and NPHS1 to monitor the differentiation process to tubular and glomerular structures and optimize maturity. The convergence of "personalized" kidney organoids with genome editing and single-cell sequencing technology hold great promise to result in better insight to disease, better human cell disease models, more predictive toxicology, and potentially "clinical trials in a dish."
MeSH term(s)	Drug Discovery ; Gene Editing ; Humans ; Induced Pluripotent Stem Cells/cytology ; Organoids/cytology ; Pluripotent Stem Cells/cytology
Language	English
Publishing date	2018-11-21
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2018.07.029
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Article ; Online: Directed differentiation of ureteric bud and collecting duct organoids from human pluripotent stem cells.

Shi, Min / Fu, Ping / Bonventre, Joseph V / McCracken, Kyle W

Nature protocols

2023 Volume 18, Issue 8, Page(s) 2485–2508

Abstract: Developing models of human kidney tissue in vitro is an important challenge in regenerative nephrology research, given the paucity of novel and effective therapies in kidney disease. However, the de novo generation of kidney tissues from human ... ...

Abstract	Developing models of human kidney tissue in vitro is an important challenge in regenerative nephrology research, given the paucity of novel and effective therapies in kidney disease. However, the de novo generation of kidney tissues from human pluripotent stem cells (hPSCs) is challenging owing to the structural and functional complexity of the organ, as well its developmental origin from two distinct embryologic populations: the metanephric mesenchyme and the ureteric bud (UB). Directed differentiation strategies have been developed to generate kidney organoids containing nephron-like structures; we recently reported an efficient and practical method to generate UB tissues. Here, we describe a detailed step-by-step protocol for differentiation of hPSCs into three-dimensonal UB organoids that exhibit complex morphological development and the capacity to differentiate into functional collecting duct tissues. Over 3 d, hPSCs are induced into PAX2
MeSH term(s)	Humans ; Kidney ; Organoids ; Pluripotent Stem Cells ; Cell Differentiation ; Tissue Engineering/methods
Language	English
Publishing date	2023-07-17
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2244966-8
ISSN	1750-2799 ; 1754-2189
ISSN (online)	1750-2799
ISSN	1754-2189
DOI	10.1038/s41596-023-00847-2
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Article ; Online: Energy depletion by cell proliferation sensitizes the kidney epithelial cells to injury.

Galichon, Pierre / Lannoy, Morgane / Li, Li / Serre, Justine / Vandermeersch, Sophie / Legouis, David / Valerius, M Todd / Hadchouel, Juliette / Bonventre, Joseph V

American journal of physiology. Renal physiology

2024 Volume 326, Issue 3, Page(s) F326–F337

Abstract: Acute kidney injury activates both proliferative and antiproliferative pathways, the consequences of which are not fully elucidated. If an initial proliferation of the renal epithelium is necessary for the successful repair, the persistence of ... ...

Abstract	Acute kidney injury activates both proliferative and antiproliferative pathways, the consequences of which are not fully elucidated. If an initial proliferation of the renal epithelium is necessary for the successful repair, the persistence of proliferation markers is associated with the occurrence of chronic kidney disease. We hypothesized that proliferation in stress conditions impacts cell viability and renal outcomes. We found that proliferation is associated with cell death after various stresses in kidney cells. In vitro, the ATP/ADP ratio oscillates reproducibly throughout the cell cycle, and cell proliferation is associated with a decreased intracellular ATP/ADP ratio. In vivo, transcriptomic data from transplanted kidneys revealed that proliferation was strongly associated with a decrease in the expression of the mitochondria-encoded genes of the oxidative phosphorylation pathway, but not of the nucleus-encoded ones. These observations suggest that mitochondrial function is a limiting factor for energy production in proliferative kidney cells after injury. The association of increased proliferation and decreased mitochondrial function was indeed associated with poor renal outcomes. In summary, proliferation is an energy-demanding process impairing the cellular ability to cope with an injury, highlighting proliferative repair and metabolic recovery as indispensable and interdependent features for successful kidney repair.
MeSH term(s)	Humans ; Kidney/metabolism ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Epithelial Cells/metabolism ; Cell Proliferation ; Adenosine Triphosphate/metabolism ; Reperfusion Injury/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2024-01-11
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.00023.2023
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Article ; Online: Acute kidney injury and maladaptive tubular repair leading to renal fibrosis.

Yu, Samuel M-W / Bonventre, Joseph V

Current opinion in nephrology and hypertension

2021 Volume 29, Issue 3, Page(s) 310–318

Abstract: Purpose of review: Despite improvements in acute kidney injury (AKI) detection, therapeutic options to halt the progression of AKI to chronic kidney disease (CKD) remain limited. In this review, we focus on recent discoveries related to the ... ...

Abstract	Purpose of review: Despite improvements in acute kidney injury (AKI) detection, therapeutic options to halt the progression of AKI to chronic kidney disease (CKD) remain limited. In this review, we focus on recent discoveries related to the pathophysiology of the AKI to CKD continuum, particularly involving the renal tubular epithelial cells, and also discuss related ongoing clinical trials. While our focus is on injured renal tubular epithelial cells as initiators of the cascade of events resulting in paracrine effects on other cells of the kidney, the summation of maladaptive responses from various kidney cell types ultimately leads to fibrosis and dysfunction characteristic of CKD. Recent findings: Recent findings that we will focus on include, but are not limited to, characterizations of: the association between cell cycle arrest and cellular senescence in renal tubular epithelial cells and its contribution to renal fibrosis, chronic inflammation with persistent cytokine production and lymphocyte infiltration among unrepaired renal tubules, mitochondrial dysfunction and a unique role of cytosolic mitochondria DNA in fibrogenesis, prolyl hydroxylase domain proteins as potential therapeutic targets, and novel mechanisms involving the Hippo/yes-associated protein/transcriptional coactivator with PDZ-binding pathway. Summary: Potential therapeutic options to address CKD progression will be informed by a better understanding of fibrogenic pathways. Recent advances suggest additional drug targets in the various pathways leading to fibrosis.
MeSH term(s)	Acute Kidney Injury/complications ; Acute Kidney Injury/physiopathology ; Animals ; Disease Progression ; Fibrosis ; Humans ; Kidney/pathology ; Kidney Tubules/physiopathology ; Renal Insufficiency, Chronic/etiology
Language	English
Publishing date	2021-04-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000605
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Zs.A 3686: Show issues

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Article ; Online: Recent advances in acute kidney injury and its consequences and impact on chronic kidney disease.

Zuk, Anna / Bonventre, Joseph V

Current opinion in nephrology and hypertension

2019 Volume 28, Issue 4, Page(s) 397–405

Abstract: Purpose of review: Acute kidney injury (AKI) remains a major unmet medical need and associates with high morbidity, mortality, and healthcare costs. Among survivors, long-term outcomes of AKI can include development of chronic kidney disease (CKD) or ... ...

Abstract	Purpose of review: Acute kidney injury (AKI) remains a major unmet medical need and associates with high morbidity, mortality, and healthcare costs. Among survivors, long-term outcomes of AKI can include development of chronic kidney disease (CKD) or progression of preexisting CKD. In this review, we focus on ongoing efforts by the AKI community to understand the human AKI to CKD continuum, with an emphasis on the cellular stress responses that underlie AKI and the maladaptive responses that persist in the acute-to-chronic phase. The emphasis is on work that has been published in the past year in this rapidly expanding field. Recent findings: Recent studies in preclinical models highlight the importance of mitochondrial dysfunction, cell death, and inflammation on the underlying pathogenesis of AKI. These pathogenic mechanisms can resolve with adaptive kidney repair but persist in maladaptive repair that leads to progressive chronic disease. The complexity and interconnections of these pathways involve cross-talk between the tubular epithelium, endothelium, and interstitial compartments. Summary: Approaches which lessen or counteract these cellular responses represent novel strategies to prevent AKI and stop or slow down the progression to CKD.
MeSH term(s)	Acute Kidney Injury/complications ; Disease Progression ; Humans ; Kidney/physiopathology ; Renal Insufficiency, Chronic/etiology
Language	English
Publishing date	2019-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000504
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Article: Primary proximal tubule injury leads to epithelial cell cycle arrest, fibrosis, vascular rarefaction, and glomerulosclerosis.

Bonventre, Joseph V

Kidney international supplements

2015 Volume 4, Issue 1, Page(s) 39–44

Abstract: Tubular injury has a major etiological role in fibrosis. For many years, this relationship has been dominated by the perception that epithelial cells are transformed into myofibroblasts that proliferate and generate fibrotic matrix-the so-called ... ...

Abstract	Tubular injury has a major etiological role in fibrosis. For many years, this relationship has been dominated by the perception that epithelial cells are transformed into myofibroblasts that proliferate and generate fibrotic matrix-the so-called epithelial-to-mesenchymal transition. Here we focus on mechanisms by which injury to the tubule results in fibrosis because of paracrine mechanisms. Specific injury to the proximal tubule results in inflammation, reversible injury, and adaptive repair if the insult is mild, self-limited in time, and occurs in a background of a normal kidney. Repeated injury, in contrast, leads to maladaptive repair with sustained tubule injury, chronic inflammation, proliferation of interstitial myofibroblasts, vascular rarefaction, interstitial fibrosis, and glomerular sclerosis. During the maladaptive repair process after the renal insult, many tubular cells become arrested in the G2/M phase of the cell cycle. This results in activation of the DNA repair response with the resultant synthesis and secretion of pro-fibrotic factors. Pharmacologic interventions that enhance the movement through G2/M or facilitate apoptosis of cells that otherwise would be blocked in G2/M may reduce the development of fibrosis after kidney injury and reduce the progression of chronic kidney disease.
Language	English
Publishing date	2015-08-25
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	193442-9
ISSN	2157-1716 ; 2157-1724 ; 0098-6577
ISSN (online)	2157-1716
ISSN	2157-1724 ; 0098-6577
DOI	10.1038/kisup.2014.8
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Zs.A 797 -Suppl.-: Show issues

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Article: Kidney injury molecule-1: a translational journey.

Bonventre, Joseph V

Transactions of the American Clinical and Climatological Association

2014 Volume 125, Page(s) 293–9; discussion 299

Abstract: Kidney injury molecule-1 (KIM-1, also named TIM-1 and HAVCR-1) was identified as the most highly upregulated protein in the proximal tubule of the kidney after injury. This protein is present with injury in multiple species including man, and also after ... ...

Abstract	Kidney injury molecule-1 (KIM-1, also named TIM-1 and HAVCR-1) was identified as the most highly upregulated protein in the proximal tubule of the kidney after injury. This protein is present with injury in multiple species including man, and also after a large number of acute and chronic insults to the kidney. It is a type-1 membrane protein whose ectodomain is released into the lumen of the tubule. The ectodomain is heavily glycosylated and stable and appears in the urine after injury. It has been qualified by the United States Food and Drug Administration and the European Medicines Agency for preclinical assessment of nephrotoxicity and on a case-by-case basis for clinical evaluation. As a biomarker in humans, its utility has been demonstrated in acute and chronic injury and in renal cell carcinoma, a condition similar to injury, where there is dedifferentiation of the epithelial cell. KIM-1 is a phosphatidylserine receptor which recognizes apoptotic cells directing them to lysosomes. It also serves as a receptor for oxidized lipoproteins and hence is important for uptake of components of the tubular lumen which may be immunomodulatory and/or toxic to the cell. KIM-1 is unique in being the first molecule, not also present on myeloid cells, that transforms kidney proximal epithelial cells into semi-professional phagocytes. Data suggest that KIM-1 expression is protective during early injury, whereas in chronic disease states, prolonged KIM-1 expression may be maladaptive and may represent a target for therapy of chronic kidney disease.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/physiopathology ; Animals ; Biomarkers/metabolism ; Hepatitis A Virus Cellular Receptor 1 ; Humans ; Kidney/metabolism ; Kidney/physiopathology ; Membrane Glycoproteins/metabolism ; Predictive Value of Tests ; Prognosis ; Receptors, Virus/metabolism ; Signal Transduction ; Translational Medical Research
Chemical Substances	Biomarkers ; HAVCR1 protein, human ; Hepatitis A Virus Cellular Receptor 1 ; Membrane Glycoproteins ; Receptors, Virus
Language	English
Publishing date	2014-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603823-2
ISSN	0065-7778
ISSN	0065-7778
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Zs.B 4: Show issues

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Article ; Online: Maladaptive proximal tubule repair: cell cycle arrest.

Bonventre, Joseph V

Nephron. Clinical practice

2014 Volume 127, Issue 1-4, Page(s) 61–64

Abstract: Acute kidney injury (AKI) leads to worsening of chronic kidney disease (CKD), and CKD predisposes to the clinical entity of AKI. The tubules of the kidney play a central role in the fibrotic response, which ultimately leads to progressive kidney disease. ...

Abstract	Acute kidney injury (AKI) leads to worsening of chronic kidney disease (CKD), and CKD predisposes to the clinical entity of AKI. The tubules of the kidney play a central role in the fibrotic response, which ultimately leads to progressive kidney disease. The cellular mechanisms responsible for the epidemiological association between AKI and CKD are complex. In order to unravel characteristics of this direct involvement of the tubules, in particular the proximal tubules, we established a model to specifically target injury to the proximal tubule using a genetic approach to express the simian diphtheria toxin (DT) receptor in the proximal tubule. A single administration of DT to the proximal tubule resulted in inflammation, reversible injury, and adaptive repair. By contrast, thrice repeated injury led to maladaptive repair with sustained tubule injury, vascular rarefaction, proliferation of interstitial myofibroblasts, interstitial fibrosis, and glomerular sclerosis. An important feature of the maladaptive repair process after severe injury is the development of cell cycle arrest in G2/M. There is a subsequent activation of the DNA repair response with activation of a secretory phenotype whereby profibrotic factors are released. This insight introduces a number of potential new targets for therapeutic intervention to prevent and/or arrest CKD progression.
MeSH term(s)	Acute Kidney Injury/complications ; Acute Kidney Injury/physiopathology ; Acute Kidney Injury/therapy ; Animals ; Cellular Senescence ; Chromatin/metabolism ; Cytokines/biosynthesis ; Cytokines/genetics ; DNA Repair ; Diphtheria Toxin/toxicity ; Disease Susceptibility ; Epithelial Cells/pathology ; Fibrosis ; G2 Phase ; Gene Expression Profiling ; Genes, Synthetic ; Heparin-binding EGF-like Growth Factor/genetics ; Humans ; Intercellular Signaling Peptides and Proteins/biosynthesis ; Intercellular Signaling Peptides and Proteins/genetics ; Kidney/blood supply ; Kidney Glomerulus/pathology ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/pathology ; Kidney Tubules, Proximal/physiopathology ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/physiology ; Metaphase ; Mice ; Molecular Targeted Therapy ; Regeneration ; Renal Insufficiency, Chronic/complications ; Renal Replacement Therapy ; Reperfusion Injury/physiopathology
Chemical Substances	Chromatin ; Cytokines ; Diphtheria Toxin ; Heparin-binding EGF-like Growth Factor ; Intercellular Signaling Peptides and Proteins
Language	English
Publishing date	2014
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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	10.1159/000363673
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