Cellular plasticity in kidney injury and repair

2016 ◽  
Vol 13 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Monica Chang-Panesso ◽  
Benjamin D. Humphreys
Keyword(s):  
Kidney Injury ◽  
Cellular Plasticity ◽  
Injury And Repair

scholarly journals Autophagy in Acute Kidney Injury and Repair

2014 ◽  
Vol 127 (1-4) ◽  
pp. 56-60 ◽  
Author(s):  
Liyu He ◽  
Man J. Livingston ◽  
Zheng Dong
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Injury And Repair

scholarly journals Recent Insights into Kidney Injury and Repair from Transcriptomic Analyses

Nephron ◽  
2019 ◽  
Vol 143 (3) ◽  
pp. 162-165 ◽  
Author(s):  
Yuhei Kirita ◽  
Monica Chang-Panesso ◽  
Benjamin D. Humphreys
Keyword(s):  
Kidney Injury ◽  
Injury And Repair

WNT–β-catenin signalling — a versatile player in kidney injury and repair

2020 ◽  
Author(s):  
Stefan J. Schunk ◽  
Jürgen Floege ◽  
Danilo Fliser ◽  
Thimoteus Speer
Keyword(s):  
Kidney Injury ◽  
Injury And Repair

scholarly journals Fibrinogen β–derived Bβ15-42 peptide protects against kidney ischemia/ reperfusion injury

Blood ◽  
2011 ◽  
Vol 118 (7) ◽  
pp. 1934-1942 ◽  
Author(s):  
Aparna Krishnamoorthy ◽  
Amrendra Kumar Ajay ◽  
Dana Hoffmann ◽  
Tae-Min Kim ◽  
Victoria Ramirez ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
High Sensitivity ◽  
Kidney Damage ◽  
Therapeutic Interventions ◽  
Mrna Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Injury And Repair

AbstractIschemia/reperfusion (I/R) injury in the kidney is a major cause of acute kidney injury (AKI) in humans and is associated with significantly high mortality. To identify genes that modulate kidney injury and repair, we conducted genome-wide expression analysis in the rat kidneys after I/R and found that the mRNA levels of fibrinogen (Fg)α, Fgβ, and Fgγ chains significantly increase in the kidney and remain elevated throughout the regeneration process. Cellular characterization of Fgα and Fgγ chain immunoreactive proteins shows a predominant expression in renal tubular cells and the localization of immunoreactive Fgβ chain protein is primarily in the renal interstitium in healthy and regenerating kidney. We also show that urinary excretion of Fg is massively increased after kidney damage and is capable of distinguishing human patients with acute or chronic kidney injury (n = 25) from healthy volunteers (n = 25) with high sensitivity and specificity (area under the receiver operating characteristic of 0.98). Furthermore, we demonstrate that Fgβ-derived Bβ15-42 peptide administration protects mice from I/R-induced kidney injury by aiding in epithelial cell proliferation and tissue repair. Given that kidney regeneration is a major determinant of outcome for patients with kidney damage, these results provide new opportunities for the use of Fg in diagnosis, prevention, and therapeutic interventions in kidney disease.

scholarly journals Non-coding RNAs in kidney injury and repair

2019 ◽  
Vol 317 (2) ◽  
pp. C177-C188 ◽  
Author(s):  
Zhiwen Liu ◽  
Ying Wang ◽  
Shaoqun Shu ◽  
Juan Cai ◽  
Chengyuan Tang ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Cell Injury ◽  
Kidney Injury ◽  
Tubular Epithelial Cell ◽  
Future Research ◽  
Circular Rnas ◽  
Rapid Decline ◽  
Rna Molecules ◽  
Non Coding Rnas ◽  
Injury And Repair

Acute kidney injury (AKI) is a major kidney disease featured by a rapid decline of renal function. Pathologically, AKI is characterized by tubular epithelial cell injury and death. Besides its acute consequence, AKI contributes critically to the development and progression of chronic kidney disease (CKD). After AKI, surviving tubular cells regenerate to repair. Normal repair restores tubular integrity, while maladaptive or incomplete repair results in renal fibrosis and eventually CKD. Non-coding RNAs (ncRNAs) are functional RNA molecules that are transcribed from DNA but not translated into proteins, which mainly include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), small nucleolar RNAs (snoRNAs), and tRNAs. Accumulating evidence suggests that ncRNAs play important roles in kidney injury and repair. In this review, we summarize the recent advances in the understanding of the roles of ncRNAs, especially miRNAs and lncRNAs in kidney injury and repair, discuss the potential application of ncRNAs as biomarkers of AKI as well as therapeutic targets for treating AKI and impeding AKI-CKD transition, and highlight the future research directions of ncRNAs in kidney injury and repair.

T Lymphocytes in Acute Kidney Injury and Repair

2020 ◽  
Vol 40 (2) ◽  
pp. 114-125
Author(s):  
Somayeh Gharaie Fathabad ◽  
Johanna T. Kurzhagen ◽  
Mohanraj Sadasivam ◽  
Sanjeev Noel ◽  
Errol Bush ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
T Lymphocytes ◽  
Kidney Injury ◽  
Injury And Repair

scholarly journals Postangiography Increases in Serum Creatinine and Biomarkers of Injury and Repair

2020 ◽  
Vol 15 (9) ◽  
pp. 1240-1250 ◽  
Author(s):  
Caroline Liu ◽  
Maria K. Mor ◽  
Paul M. Palevsky ◽  
James S. Kaufman ◽  
Heather Thiessen Philbrook ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Serious Adverse Events ◽  
Monocyte Chemoattractant Protein 1 ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Iodinated Contrast ◽  
Injury And Repair ◽  
Kidney Injury Molecule 1 ◽  
Major Adverse Kidney Events

Background and objectivesIt is unknown whether iodinated contrast causes kidney parenchymal damage. Biomarkers that are more specific to nephron injury than serum creatinine may provide insight into whether contrast-associated AKI reflects tubular damage. We assessed the association between biomarker changes after contrast angiography with contrast-associated AKI and 90-day major adverse kidney events and death.Design, setting, participants, & measurementsWe conducted a longitudinal analysis of participants from the biomarker substudy of the Prevention of Serious Adverse Events following Angiography trial. We measured injury (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, IL-18) and repair (monocyte chemoattractant protein-1, uromodulin, YKL-40) proteins from plasma and urine samples at baseline and 2–4 hours postangiography. We assessed the associations between absolute changes and relative ratios of biomarkers with contrast-associated AKI and 90-day major adverse kidney events and death.ResultsParticipants (n=922) were predominately men (97%) with diabetes (82%). Mean age was 70±8 years, and eGFR was 48±13 ml/min per 1.73 m2; 73 (8%) and 60 (7%) participants experienced contrast-associated AKI and 90-day major adverse kidney events and death, respectively. No postangiography urine biomarkers were associated with contrast-associated AKI. Postangiography plasma kidney injury molecule-1 and IL-18 were significantly higher in participants with contrast-associated AKI compared with those who did not develop contrast-associated AKI: 428 (248, 745) versus 306 (179, 567) mg/dl; P=0.04 and 325 (247, 422) versus 280 (212, 366) mg/dl; P=0.009, respectively. The majority of patients did not experience an increase in urine or plasma biomarkers. Absolute changes in plasma IL-18 were comparable in participants with contrast-associated AKI (−30 [−71, −9] mg/dl) and those without contrast-associated AKI (−27 [−53, −10] mg/dl; P=0.62). Relative ratios of plasma IL-18 were also comparable in participants with contrast-associated AKI (0.91; 0.86, 0.97) and those without contrast-associated AKI (0.91; 0.85, 0.96; P=0.54).ConclusionsThe lack of significant differences in the absolute changes and relative ratios of injury and repair biomarkers by contrast-associated AKI status suggests that the majority of mild contrast-associated AKI cases may be driven by hemodynamic changes at the kidney.

scholarly journals FoxM1 drives proximal tubule proliferation during repair from acute kidney injury

2018 ◽  
Author(s):  
Monica Chang-Panesso ◽  
Farid F. Kadyrov ◽  
Matthew Lalli ◽  
Haojia Wu ◽  
Shiyo Ikeda ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Molecular Mechanisms ◽  
Growth Factor Receptor ◽  
Kidney Injury ◽  
Acute Injury ◽  
Genetic Lineage ◽  
Proximal Tubule Cells ◽  
Epidermal Growth ◽  
Tubule Cells ◽  
Injury And Repair

AbstractThe proximal tubule has a remarkable capacity for repair after acute injury but the cellular lineage and molecular mechanisms underlying this repair response have been poorly characterized. Here, we developed a Kim-1-GFPCreERt2knockin mouse line (Kim-1-GCE), performed genetic lineage analysis after injury and measured the cellular transcriptome of proximal tubule during repair. Acutely injured genetically labeled clones co-expressed Kim-1, Vimentin, Sox9 and Ki67, indicating a dedifferentiated and proliferative state. Clonal analysis revealed clonal expansion of Kim-1+ cells, indicating that acutely injured, dedifferentiated proximal tubule cells account for repair rather than a fixed tubular progenitor. Translational profiling during injury and repair revealed signatures of both successful and unsuccessful maladaptive repair. The transcription factor FoxM1 was induced early in injury, was required for epithelial proliferation, and was dependent on epidermal growth factor receptor (EGFR) stimulation. In conclusion, dedifferentiated proximal tubule cells effect proximal tubule repair and we reveal a novel EGFR-FoxM1-dependent signaling pathway that drives proliferative repair after injury.

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