The future role of proteomics in the understanding of acute kidney injury

Bennett, Michael; Devarajan, Prasad

doi:10.1080/14789450.2018.1443007

Cited by 7 publications

(5 citation statements)

References 12 publications

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“…Biomarkers of acute kidney injury. Most of the biomarkers of renal damage characterized in the field of AKI and DGF, such as neutrophil gelatinase-associated lipocain (NGAL) and kidney injury molecule-1 (KIM-1), are associated with tubular injury (9,99). Neither KIM-1 nor NGAL have shown any association with ulterior graft function in patients with DGF (85).…”

Section: Ischemia-reperfusion Injury To the Kidney Graft Microcirculation And Relevant Biomarkersmentioning

confidence: 99%

The determinants, biomarkers, and consequences of microvascular injury in kidney transplant recipients

Doreille

Dieudé

Cardinal

2019

American Journal of Physiology-Renal Physiology

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Independent of the initial cause of kidney disease, microvascular injury to the peritubular capillary network appears to play a central role in the development of interstitial fibrosis in both native and transplanted kidney disease. This association is explained by mechanisms such as the upregulation of profibrotic genes and epigenetic changes induced by hypoxia, capillary leakage, endothelial and pericyte transition to interstitial fibroblasts, as well as modifications in the secretome of endothelial cells. Alloimmune injury due to antibody-mediated rejection and ischemia-reperfusion injury are the two main etiologies of microvascular damage in kidney transplant recipients. The presence of circulating donor-specific anti-human leukocyte antigen (HLA) antibodies, histological findings, such as diffuse C4d staining in peritubular capillaries, and the extent and severity of peritubular capillaritis, are commonly used clinically to provide both diagnostic and prognostic information. Complement-dependent assays, circulating non-HLA antibodies, or evaluation of the microvasculature with novel imaging techniques are the subject of ongoing studies.

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Section: Ischemia-reperfusion Injury To the Kidney Graft Microcirculation And Relevant Biomarkersmentioning

confidence: 99%

The determinants, biomarkers, and consequences of microvascular injury in kidney transplant recipients

Doreille

Dieudé

Cardinal

2019

American Journal of Physiology-Renal Physiology

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“…Current diagnostic tools do not allow early detection or prediction of the course of AKI, thereby hampering any improvement in patient outcome [49]. The search for biomarkers predicting progression to severe damage has come up with substances that exhibit the presence of AKI but are of limited success in differentiating severe AKI from less severe forms [50]. Most of these biomarkers are closely linked to a single pathologic process, so that they perform poorly in AKI populations with other pathophysiological mechanisms or heterogeneous origins [49].…”

Section: Acute Kidney Injurymentioning

confidence: 99%

Urinary Peptidomic Biomarkers in Kidney Diseases

Sirolli

Pieroni

Liberato

et al. 2019

IJMS

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In order to effectively develop personalized medicine for kidney diseases we urgently need to develop highly accurate biomarkers for use in the clinic, since current biomarkers of kidney damage (changes in serum creatinine and/or urine albumin excretion) apply to a later stage of disease, lack accuracy, and are not connected with molecular pathophysiology. Analysis of urine peptide content (urinary peptidomics) has emerged as one of the most attractive areas in disease biomarker discovery. Urinary peptidome analysis allows the detection of short and long-term physiological or pathological changes occurring within the kidney. Urinary peptidomics has been applied extensively for several years now in renal patients, and may greatly improve kidney disease management by supporting earlier and more accurate detection, prognostic assessment, and prediction of response to treatment. It also promises better understanding of kidney disease pathophysiology, and has been proposed as a "liquid biopsy" to discriminate various types of renal disorders. Furthermore, proteins being the major drug targets, peptidome analysis may allow one to evaluate the effects of therapies at the protein signaling pathway level. We here review the most recent findings on urinary peptidomics in the setting of the most common kidney diseases.

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“…It is a powerful tool for detecting targets in response to drug therapy/toxicity by monitoring changes in protein expression, and the strategy for discovering targets is to compare differentially expressed proteins (DEPs) in biological samples, which reflect the progress of in vivo toxicity or are used as prognostic markers ( Titz et al, 2014 ). Recently the method is more and more widely used to explore the pharmacological and toxicological mechanisms of herbs ( Bennett and Devarajan, 2018 ). Label-free quantitative method is one of the important applications in the field of proteomics research.…”

Section: Introductionmentioning

confidence: 99%

Delineation of renal protein profiles in aristolochic acid I-induced nephrotoxicity in mice by label-free quantitative proteomics

Liu,

Wu,

Peng

et al. 2024

Front. Pharmacol.

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Introduction: Aristolochic acid nephropathy (AAN) is a kidney injury syndrome caused by aristolochic acids exposure. Our study used label-free quantitative proteomics to delineate renal protein profiles and identify key proteins after exposure to different doses of aristolochic acid I (AAI).Methods: Male C57BL/6 mice received AAI (1.25 mg/kg/d, 2.5 mg/kg/d, or 5 mg/kg/d) or vehicle for 5 days.Results and discussion: The results showed that AAI induced dose-dependent nephrotoxicity. Differences in renal protein profiles between the control and AAI groups increased with AAI dose. Comparing the control with the low-, medium-, and high-dose AAI groups, we found 58, 210, and 271 differentially expressed proteins, respectively. Furthermore, protein-protein interaction network analysis identified acyl-CoA synthetase medium-chain family member 3 (Acsm3), cytochrome P450 family 2 subfamily E member 1 (Cyp2e1), microsomal glutathione S-transferase 1 (Mgst1), and fetuin B (Fetub) as the key proteins. Proteomics revealed that AAI decreased Acsm3 and Cyp2e1 while increasing Mgst1 and Fetub expression in mice kidneys, which was further confirmed by Western blotting. Collectively, in AAI-induced nephrotoxicity, renal protein profiles were dysregulated and exacerbated with increasing AAI dose. Acsm3, Cyp2e1, Mgst1, and Fetub may be the potential therapeutic targets for AAN.

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The future role of proteomics in the understanding of acute kidney injury

Cited by 7 publications

References 12 publications

The determinants, biomarkers, and consequences of microvascular injury in kidney transplant recipients

The determinants, biomarkers, and consequences of microvascular injury in kidney transplant recipients

Urinary Peptidomic Biomarkers in Kidney Diseases

Delineation of renal protein profiles in aristolochic acid I-induced nephrotoxicity in mice by label-free quantitative proteomics

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