scholarly journals Kidney Inflammation, Injury and Regeneration

2020 ◽  
Vol 21 (3) ◽  
pp. 1164 ◽  
Author(s):  
Baer ◽  
Koch ◽  
Geiger
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Kidney Injury ◽  
Kidney Cells

Damage to kidney cells can occur due to a variety of ischemic and toxic insults and leads to inflammation and cell death, which can result in acute kidney injury (AKI) [...]

scholarly journals Mechanisms of LPS-Induced Acute Kidney Injury in Neonatal and Adult Rats

Antioxidants ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 105 ◽  
Author(s):  
Egor Plotnikov ◽  
Anna Brezgunova ◽  
Irina Pevzner ◽  
Ljubava Zorova ◽  
Vasily Manskikh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Smooth Muscle Actin ◽  
Accelerated Aging ◽  
Kidney Injury ◽  
Nuclear Antigen ◽  
Kidney Cells ◽  
Adult Rats ◽  
Mortality And Morbidity ◽  
Causes Of Mortality

Neonatal sepsis is one of the major causes of mortality and morbidity in newborns, greatly associated with severe acute kidney injury (AKI) and failure. Handling of newborns with kidney damage can be significantly different compared to adults, and it is necessary to consider the individuality of an organism’s response to systemic inflammation. In this study, we used lipopolysaccharide (LPS)-mediated acute kidney injury model to study mechanisms of kidney cells damage in neonatal and adult rats. We found LPS-associated oxidative stress was more severe in adults compared to neonates, as judged by levels of carbonylated proteins and products of lipids peroxidation. In both models, LPS-mediated septic simulation caused apoptosis of kidney cells, albeit to a different degree. Elevated levels of proliferating cell nuclear antigen (PCNA) in the kidney dropped after LPS administration in neonates but increased in adults. Renal fibrosis, as estimated by smooth muscle actin levels, was significantly higher in adult kidneys, whereas these changes were less profound in LPS-treated neonatal kidneys. We concluded that in LPS-mediated AKI model, renal cells of neonatal rats were more tolerant to oxidative stress and suffered less from long-term pathological consequences, such as fibrosis. In addition, we assume that by some features LPS administration simulates the conditions of accelerated aging.

Pathogenesis of Acute Kidney Injury

2019 ◽  
pp. 11-20
Author(s):  
David P. Basile ◽  
Babu J. Padanilam
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Renal Function ◽  
Fatty Acid ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Acid Oxidation ◽  
Clinical Disorder ◽  
Successful Recovery ◽  
Multiple Issues

Acute kidney injury represents a significant clinical disorder associated with a rapid loss of renal function following a variety of potential insults. This chapter reviews multiple issues related to the pathophysiology of AKI with an emphasis on studies from animal models. Early responses following kidney injury include impaired hemodynamic and bioenergetic responses. Reductions in renal ATP levels occur as a result of compromised fatty acid oxidation and impaired compensation by glycolysis. Sustained reductions in perfusion contribute to extension of AKI characterized by complex inflammatory and cellular injury responses, often leading to cell death. Concurrently, the kidney displays an elegant repair response, leading to successful recovery in most cases, characterized in part by epithelial cell growth, while maladaptive or incomplete recovery of tubules or capillaries can predispose the development of interstitial fibrosis and CKD progression.

scholarly journals Programmed cell death protein 1 inhibitor treatment is associated with acute kidney injury and hypocalcemia: meta-analysis

2018 ◽  
Vol 34 (1) ◽  
pp. 108-117 ◽  
Author(s):  
Sandhya Manohar ◽  
Panagiotis Kompotiatis ◽  
Charat Thongprayoon ◽  
Wisit Cheungpasitporn ◽  
Joerg Herrmann ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Meta Analysis ◽  
Kidney Injury ◽  
Cell Death Protein ◽  
Inhibitor Treatment

scholarly journals Cell Death Patterns Due to Warm Ischemia or Reperfusion in Renal Tubular Epithelial Cells Originating from Human, Mouse, or the Native Hibernator Hamster

Biology ◽  
2018 ◽  
Vol 7 (4) ◽  
pp. 48 ◽  
Author(s):  
Theodoros Eleftheriadis ◽  
Georgios Pissas ◽  
Georgia Antoniadi ◽  
Vassilios Liakopoulos ◽  
Ioannis Stefanidis
Keyword(s):  
Lipid Peroxidation ◽  
Acute Kidney Injury ◽  
Cell Death ◽  
Epithelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Human Cells ◽  
Tubular Epithelial Cells

Ischemia–reperfusion injury contributes to the pathogenesis of many diseases, with acute kidney injury included. Hibernating mammals survive prolonged bouts of deep torpor with a dramatic drop in blood pressure, heart, and breathing rates, interspersed with short periods of arousal and, consequently, ischemia–reperfusion injury. Clarifying the differences under warm anoxia or reoxygenation between human cells and cells from a native hibernator may reveal interventions for rendering human cells resistant to ischemia–reperfusion injury. Human and hamster renal proximal tubular epithelial cells (RPTECs) were cultured under warm anoxia or reoxygenation. Mouse RPTECs were used as a phylogenetic control for hamster cells. Cell death was assessed by both cell imaging and lactate dehydrogenase (LDH) release assay, apoptosis by cleaved caspase-3, autophagy by microtubule-associated protein 1-light chain 3 B II (LC3B-II) to LC3B-I ratio, necroptosis by phosphorylated mixed-lineage kinase domain-like pseudokinase, reactive oxygen species (ROS) fluorometrically, and lipid peroxidation, the end-point of ferroptosis, by malondialdehyde. Human cells died after short periods of warm anoxia or reoxygenation, whereas hamster cells were extremely resistant. In human cells, apoptosis contributed to cell death under both anoxia and reoxygenation. Although under reoxygenation, ROS increased in both human and hamster RPTECs, lipid peroxidation-induced cell death was detected only in human cells. Autophagy was observed only in human cells under both conditions. Necroptosis was not detected in any of the evaluated cells. Clarifying the ways that are responsible for hamster RPTECs escaping from apoptosis and lipid peroxidation-induced cell death may reveal interventions for preventing ischemia–reperfusion-induced acute kidney injury in humans.

scholarly journals MDM2 prevents spontaneous tubular epithelial cell death and acute kidney injury

2016 ◽  
Vol 7 (11) ◽  
pp. e2482-e2482 ◽  
Author(s):  
Dana Thomasova ◽  
Martrez Ebrahim ◽  
Kristina Fleckinger ◽  
Moying Li ◽  
Jakob Molnar ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Epithelial Cell ◽  
Kidney Injury ◽  
Tubular Epithelial Cell ◽  
Epithelial Cell Death

scholarly journals Cell Death Pathways Drive Necroinflammation during Acute Kidney Injury

Nephron ◽  
2018 ◽  
Vol 140 (2) ◽  
pp. 144-147 ◽  
Author(s):  
Anne von Mässenhausen ◽  
Wulf Tonnus ◽  
Andreas Linkermann
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Kidney Injury ◽  
Cell Death Pathways

scholarly journals Caspase-11 Mediates Pyroptosis of Tubular Epithelial Cells and Septic Acute Kidney Injury

2019 ◽  
Vol 44 (4) ◽  
pp. 465-478 ◽  
Author(s):  
Zhiming Ye ◽  
Li Zhang ◽  
Ruizhao Li ◽  
Wei Dong ◽  
Shuangxin Liu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Epithelial Cells ◽  
Serum Creatinine ◽  
Protein Expression ◽  
Kidney Injury ◽  
Interleukin 1Β ◽  
Tubular Epithelial Cells

Background/Aims: Acute kidney injury (AKI) is a serious complication of sepsis and has a high morbidity and mortality rate. Caspase-11 induces pyroptosis, a form of programmed cell death that plays a critical role in endotoxic shock, but its role in tubular epithelial cell death and whether it contributes to sepsis-associated AKI remains unknown. Methods: The caspase-11–/– mouse received an intraperitoneal injection of lipopolysaccharide (LPS, 40 mg/kg body weight). Caspase-11–/– renal tubular epithelial cells (RTECs) form C57BL caspase-11–/– mice were treated with LPS in vitro. The IL-1β ELISA kit and Scr assay kit were used to measure the level of interleukin-1β and serum creatinine. Annexin V-FITC assay and TUNEL staining assay were used to detect the cell death in different groups in vitro and in vivo. Western blot was performed to analyze the protein expression of caspase-11 and Gsdmdc1. Results: LPS-induced sepsis results in lytic death of RTECs, accompanied by increased expression of the pyroptosis-related proteins caspase-11 and Gsdmd. However, the increase in pyroptosis-related protein expression induced by LPS was attenuated with caspase-11 knockout, both in vitro and in vivo. Furthermore, when challenged with lethal doses of systemic LPS, pathologic abnormalities in renal structure, increased serum and kidney interleukin-1β, increased serum creatinine, and animal death were observed in wild-type mice but prevented in caspase-11–/– mice. Conclusions: Caspase-11-induced pyroptosis of RTECs is a key event during septic AKI, and targeting of caspase-11 in RTECs may serve as a novel therapeutic target in septic AKI.

scholarly journals C-type lectin Mincle mediates cell death–triggered inflammation in acute kidney injury

2020 ◽  
Vol 217 (11) ◽  
Author(s):  
Miyako Tanaka ◽  
Marie Saka-Tanaka ◽  
Kozue Ochi ◽  
Kumiko Fujieda ◽  
Yuki Sugiura ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cell Death ◽  
Free Cholesterol ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Sterile Inflammation ◽  
Renal Tubular Cell ◽  
Renal Tubules ◽  
Underlying Mechanisms

Accumulating evidence indicates that cell death triggers sterile inflammation and that impaired clearance of dead cells causes nonresolving inflammation; however, the underlying mechanisms are still unclear. Here, we show that macrophage-inducible C-type lectin (Mincle) senses renal tubular cell death to induce sustained inflammation after acute kidney injury in mice. Mincle-deficient mice were protected against tissue damage and subsequent atrophy of the kidney after ischemia–reperfusion injury. Using lipophilic extract from the injured kidney, we identified β-glucosylceramide as an endogenous Mincle ligand. Notably, free cholesterol markedly enhanced the agonistic effect of β-glucosylceramide on Mincle. Moreover, β-glucosylceramide and free cholesterol accumulated in dead renal tubules in proximity to Mincle-expressing macrophages, where Mincle was supposed to inhibit clearance of dead cells and increase proinflammatory cytokine production. This study demonstrates that β-glucosylceramide in combination with free cholesterol acts on Mincle as an endogenous ligand to induce cell death–triggered, sustained inflammation after acute kidney injury.

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