scholarly journals Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Fei Zhao ◽  
Li-Xin Feng ◽  
Qian Liu ◽  
Hong-Shen Wang ◽  
Cheng-Yuan Tang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Quality Control ◽  
Kidney Injury ◽  
Protective Role ◽  
Mitochondrial Quality Control ◽  
Therapy Strategy ◽  
Nrf2 Signaling Pathway ◽  
Short And Long Term ◽  
Renal Tubular

Contrast-induced acute kidney injury (CI-AKI) is the third common cause of acute kidney injury (AKI), which is associated with poor short- and long-term outcomes. Currently, effective therapy strategy for CI-AKI remains lacking. Stanniocalcin-1 (STC1) is a conserved glycoprotein with antiapoptosis and anti-inflammatory functions, but the role of STC1 in controlling CI-AKI is unknown. Here, we demonstrated a protective role of STC1 in contrast-induced injury in cultured renal tubular epithelial cells and CI-AKI rat models. Recombinant human STC1 (rhSTC1) regulated mitochondrial quality control, thus suppressing contrast-induced mitochondrial damage, oxidative stress, inflammatory response, and apoptotic injury. Mechanistically, activation of the Nrf2 signaling pathway contributes critically to the renoprotective effect of STC1. Together, this study demonstrates a novel role of STC1 in preventing CI-AKI and reveals Nrf2 as a molecular target of STC1. Therefore, this study provides a promising preventive target for the treatment of CI-AKI.

Protective role of HO‐1 against acute kidney injury caused by cutaneous exposure to arsenicals

2020 ◽  
Vol 1480 (1) ◽  
pp. 155-169
Author(s):  
Ritesh K. Srivastava ◽  
Suhail Muzaffar ◽  
Jasim Khan ◽  
Amie M. Traylor ◽  
Jaroslaw W. Zmijewski ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Protective role of fructokinase blockade in the pathogenesis of acute kidney injury in mice

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Ana Andres-Hernando ◽  
Nanxing Li ◽  
Christina Cicerchi ◽  
Shinichiro Inaba ◽  
Wei Chen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Role of Intracellular Ca2+and Na+/Ca2+Exchanger in the Pathogenesis of Contrast-Induced Acute Kidney Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Dingping Yang ◽  
Dingwei Yang
Keyword(s):  
Acute Kidney Injury ◽  
Cell Injury ◽  
Kidney Injury ◽  
Renal Tubular Cell ◽  
Voltage Dependent ◽  
Key Factor ◽  
Intracellular Ca ◽  
Underlying Mechanisms ◽  
Renal Tubular

The precise mechanisms underlying contrast-induced acute kidney injury (CI-AKI) are not well understood. Intracellular Ca2+overload is considered to be a key factor in CI-AKI. Voltage-dependent Ca2+channel (VDC) and Na+/Ca2+exchanger (NCX) system are the main pathways of intracellular Ca2+overload in pathological conditions. Here, we review the potential underlying mechanisms involved in CI-AKI and discuss the role of NCX-mediated intracellular Ca2+overload in the contrast media-induced renal tubular cell injury and renal hemodynamic disorder.

scholarly journals Protective Effect of Procambarus Clarkia Hemolymph against Acute Kidney Injury Induced by Gentamicin in Rats

2020 ◽  
pp. 123-129
Author(s):  
Abdeljalil M`ohamed Al Shawoush ◽  
Ayman Saber Mohamed ◽  
Sohair Ramadan Fahmy
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role ◽  
Pharmacological Activities ◽  
Partial Restoration ◽  
Stress Markers ◽  
Study Results ◽  
Liver Functions ◽  
Kidney Functions

Background: P.clarkii hemolymph has several pharmacological activities against inflammation, bacteria and tumor. The current study aimed to explore the efficacy of P.clarkii hemolymph against the renal toxicity induced by Gentamicin (GM) in rats. Methods: The animals were divided randomly into three groups (six per group): control, GM and P.clarkii. Tissues toxicity was established after injection of GM daily for eight days at a dose 100 mg/kg. Kidney functions, liver functions, oxidative stress markers and histopathology of tissues were investigated in the study. Results: P.clarkii treated rats showed a significant decrease in urea, creatinine, uric acid, ALT, AST, and MDA levels while GSH and CAT levels increased. The histology of kidney investigation showed partial restoration of renal architecture. Conclusion: The study results revealed the protective role of p.clarkii hemolymph against gentamicin-induced acute kidney injury in rats.

The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery

2018 ◽  
Vol 10 (441) ◽  
pp. eaan4886 ◽  
Author(s):  
Christian Stoppe ◽  
Luisa Averdunk ◽  
Andreas Goetzenich ◽  
Josefin Soppert ◽  
Arnaud Marlier ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Kidney Injury ◽  
Protective Role ◽  
Inhibitory Factor ◽  
Macrophage Migration

The protective role of estrogen and its receptors in gentamicin-induced acute kidney injury in rats

Life Sciences ◽  
2019 ◽  
Vol 239 ◽  
pp. 117082
Author(s):  
Sayed M. Abd El-Lateef ◽  
El-Sayed M. El-Sayed ◽  
Ahmed M. Mansour ◽  
Salama A. Salama
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity

2019 ◽  
Vol 20 (20) ◽  
pp. 5238 ◽  
Author(s):  
Daniela Maria Tanase ◽  
Evelina Maria Gosav ◽  
Smaranda Radu ◽  
Claudia Florida Costea ◽  
Manuela Ciocoiu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
In Vivo Studies ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Induced Apoptosis ◽  
Kidney Injury Molecule 1

Acute kidney injury (AKI) following platinum-based chemotherapeutics is a frequently reported serious side-effect. However, there are no approved biomarkers that can properly identify proximal tubular injury while routine assessments such as serum creatinine lack sensitivity. Kidney-injury-molecule 1 (KIM-1) is showing promise in identifying cisplatin-induced renal injury both in vitro and in vivo studies. In this review, we focus on describing the mechanisms of renal tubular cells cisplatin-induced apoptosis, the associated inflammatory response and oxidative stress and the role of KIM-1 as a possible biomarker used to predict cisplatin associated AKI.

scholarly journals Protective role of endothelial calpain knockout in lipopolysaccharide-induced acute kidney injury via attenuation of the p38-iNOS pathway and NO/ROS production

2020 ◽  
Vol 52 (4) ◽  
pp. 702-712
Author(s):  
Zhifeng Liu ◽  
Jingjing Ji ◽  
Dong Zheng ◽  
Lei Su ◽  
Tianqing Peng ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Protective Role ◽  
Inos Expression ◽  
Calpain Inhibitor ◽  
Ros Production ◽  
Enos Expression ◽  
Cellular Apoptosis

Abstract To explore the role of calpain and its signaling pathway in lipopolysaccharide (LPS)-induced acute kidney injury (AKI), animal models of endotoxemia were established by administration of LPS to mice with endothelial-specific Capn4 knockout (TEK/Capn4−/−), mice with calpastatin (an endogenous calpain inhibitor) overexpression (Tg-CAST) and mice with myeloid-specific Capn4 knockout (LYZ/Capn4−/−). Mouse pulmonary microvascular endothelial cells (PMECs) were used as a model of the microvascular endothelium and were stimulated with LPS. Renal function, renal inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) expression, cellular apoptosis, plasma and renal levels of NO and reactive oxygen species (ROS), and phosphorylation of mitogen-activated protein kinase (MAPK) family members (p38, ERK1/2, and JNK1/2) were examined. Moreover, a calpain inhibitor, calpastatin overexpression adenoviruses and MAPK inhibitors were used. Significant renal dysfunction was induced by LPS stimulation, and recovery was observed in TEK/Capn4−/− and Tg-CAST mice but not in LYZ/Capn4−/− mice. Endothelial Capn4 knockout also abrogated the LPS-induced increases in renal iNOS expression, caspase-3 activity and apoptosis and plasma and renal NO and ROS levels but did not obviously affect renal eNOS expression. Moreover, LPS increased both calpain and caspase-3 activity, and only the expression of iNOS in PMECs was accompanied by increased phosphorylation of p38 and JNK. Inhibiting calpain activity or p38 phosphorylation alleviated the increased iNOS expression, NO/ROS production, and cellular apoptosis induced by LPS. These results suggest that endothelial calpain plays a protective role in LPS-induced AKI by inhibiting p38 phosphorylation, thus attenuating iNOS expression and further decreasing NO and ROS overproduction-induced endothelial apoptosis.

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