Acute Kidney Injury in Asia: Disease Burden

Xu, Dianqing; Yang, Li

doi:10.1016/j.semnephrol.2020.08.001

Cited by 11 publications

(7 citation statements)

References 105 publications

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“…AKI is a global disease with high incidence and mortality. Epidemiological studies have revealed the huge medical and economic burden of AKI in Eastern Asian countries [ 24 , 25 ]. Preventive opportunities are missed because of the failure to recognize risk factors and early signs of AKI 24 .…”

Section: Discussionmentioning

confidence: 99%

CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice

Huang

Peng

et al. 2023

Renal Failure

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Aim Renal tubular epithelial cell (RTEC) apoptosis is important in acute kidney injury (AKI). Calcium/calmodulin-dependent protein kinase II (CaMKII) plays an important role in cell apoptosis, but its potential role in AKI remains unknown. Methods Using co-immunoprecipitation, immunofluorescence, immunohistochemistry, western blotting, flow cytometry, and cell transfection, this study aimed to verify whether CaMKII is involved in RTEC apoptosis and to explore the underlying mechanism. Results We found that CaMKII was involved in RTEC apoptosis. In adriamycin-induced AKI mice, serum creatinine levels, cell apoptosis, CaMKII activity, and nuclear factor of activated T cells 2 (NFAT2) levels increased, whereas nuclear Yes-associated protein (YAP) expression decreased; inhibition of CaMKII activity reversed these changes. Phosphorylated CaMKII could bind to phosphorylated YAP in the cytoplasm and block it from entering the nucleus, thereby failing to inhibit NFAT2-mediated cell apoptosis. Sequestrated phosphorylated YAP in the RTEC cytoplasm was finally degraded by ubiquitination. Conclusion CaMKII may regulate RTEC apoptosis through YAP/NFAT2 in AKI mice. CaMKII may be a potent molecular target for AKI treatment.

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Section: Discussionmentioning

confidence: 99%

CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice

Huang

Peng

et al. 2023

Renal Failure

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“…The incidence of acute kidney injury has been increasing over time, with mortality remaining high in the past decades and an estimated burden higher than that of breast cancer, heart failure, and diabetes [ 42 , 43 , 44 ]. The problem of renal function is not only related to AKI, which is normally an acute condition, but also to the tendency of people who have had AKI to develop a permanent kidney injury, which then increases the risk of developing chronic kidney disease (CKD) in the future [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury (AKI) in Young Synthetic Cannabinoids Abusers

et al. 2022

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Background. Synthetic cannabinoid-related acute kidney injury represents an increasingly important public health issue due to the diagnostic challenges given by low clinical suspicion of the disease and the frequent undetectability in routine drug tests. Methods. A systematic literature search on PubMed was carried out until 31 January 2022. Case reports, case series, retrospective and prospective studies, as well as reviews on acute kidney injury related to the consumption of synthetic cannabinoid were searched. Results. The systematic review process selected 21 studies for a total of 55 subjects with synthetic cannabinoid-induced acute kidney injury. Renal damage was demonstrated by elevated serum creatinine levels in 49 patients (89%). On renal ultrasound, the most frequent finding was an increase in cortical echogenicity. Renal biopsy, performed in 33% of cases, revealed acute tubular damage, acute tubulointerstitial nephritis, and acute interstitial nephritis, in decreasing order of frequency. Conclusion. Prompt identification and treatment of synthetic cannabinoid-related acute kidney injury represent a sensitive public health goal both for the acute management of damage from synthetic cannabinoids and for the prevention of chronic kidney disease.

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“…Acute kidney injury (AKI) is defined as the sudden loss of kidney function due to the severe damage to the kidney, particularly to tubular epithelial cells. Increasing evidence shows that AKI is a major cause of chronic kidney disease (CKD) with high mortality [1][2][3]. However, effective treatments for AKI remain limited and studies on mechanisms of AKI remain challenging.…”

Section: Introductionmentioning

confidence: 99%

“…There are many risk factors for AKI, including hypertension, ischemic injury, nephrotoxic drugs, sepsis, major surgery, etc. [1][2][3]. Growing evidence shows that immune cells such as macrophages, dendritic cells, T cells, and neutrophils also participate in the pathogenesis of AKI [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y protects kidney from acute kidney injury by inactivating M1 macrophages via the Y1R-NF-κB-Mincle-dependent mechanism

Tan¹,

Li²,

Zhu³

et al. 2023

Int. J. Biol. Sci.

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Neuropeptide Y (NPY) is produced by the nerve system and may contribute to the progression of CKD. The present study found the new protective role for NPY in AKI in both patients and animal models. Interestingly, NPY was constitutively expressed in blood and resident kidney macrophages by co-expressing NPY and CD68+ markers, which was lost in patients and mice with AKI-induced by cisplatin. Unexpectedly, NPY was renoprotective in AKI as mice lacking NPY developed worse renal necroinflammation and renal dysfunction in cisplatin and ischemic-induced AKI. Importantly, NPY was also a therapeutic agent for AKI because treatment with exogenous NPY dose-dependently inhibited cisplatin-induced AKI. Mechanistically, NPY protected kidney from AKI by inactivating M1 macrophages via the Y1R-NF-κB-Mincle-dependent mechanism as deleting or silencing NPY decreased Y1R but increased NF-κB-Mincle-mediated M1macrophage activation and renal necroinflammation, which were reversed by addition of NPY or by silencing Mincle but promoted by blocking Y1R with BIBP 3226. Thus, NPY is renoprotective and may be a novel therapeutic agent for AKI. NPY may act via Y1R to protect kidney from AKI by blocking NF-κB-Mincle-mediated M1 macrophage activation and renal necroinflammation.

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Acute Kidney Injury in Asia: Disease Burden

Cited by 11 publications

References 105 publications

CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice

CaMKII may regulate renal tubular epithelial cell apoptosis through YAP/NFAT2 in acute kidney injury mice

Acute Kidney Injury (AKI) in Young Synthetic Cannabinoids Abusers

Neuropeptide Y protects kidney from acute kidney injury by inactivating M1 macrophages via the Y1R-NF-κB-Mincle-dependent mechanism

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