Distant organ dysfunction in acute kidney injury

Husain‐Syed, Faeq; Rosner, Mitchell H.; Ronco, Claudio

doi:10.1111/apha.13357

Cited by 33 publications

(24 citation statements)

References 100 publications

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“…Protein expression levels were determined via western blot as previously described [45]. After cell collection, protein lysis and extraction were performed using RIPA lysis buffer (R0278, Sigma-Aldrich, USA), and the concentration of extracted protein was measured using the Bicinchoninic acid (BCA) protein assay kit (AR0146, Boster Bio, Pleasanton, CA, USA) [46]. Then, 20 μg protein lysates samples were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE; P0012AC, Beyotime, China) and transferred onto polyvinylidene fluoride (PVDF) membranes (FFP36, Beyotime, China), which were blocked with fat-free milk (5%) for 2 hours and incubated with primary antibodies at 4°C overnight; β-actin was used as internal control [47,48].…”

Section: Mitochondrial Membrane Potential (Mmp) Assessmentmentioning

confidence: 99%

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Xie¹,

Zhong

Guo

et al. 2021

Oxidative Medicine and Cellular Longevity

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Endothelial dysfunction, which is characterized by damage to the endoplasmic reticulum (ER) and mitochondria, is involved in a variety of cardiovascular disorders. Here, we explored whether mitochondrial damage and ER stress are associated with endothelial dysfunction. We also examined whether and how melatonin protects against oxidized low-density lipoprotein- (ox-LDL-) induced damage in endothelial cells. We found that CHOP, GRP78, and PERK expressions, which are indicative of ER stress, increased significantly in response to ox-LDL treatment. ox-LDL also induced mitochondrial dysfunction as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS levels, and downregulation of mitochondrial protective factors. In addition, ox-LDL inhibited antioxidative processes, as evidenced by decreased antioxidative enzyme activity and reduced Nrf2/HO-1 expression. Melatonin clearly reduced ER stress and promoted mitochondrial function and antioxidative processes in the presence of ox-LDL. Molecular investigation revealed that ox-LDL activated the JNK/Mff signaling pathway, and melatonin blocked this effect. These results demonstrate that ox-LDL induces ER stress and mitochondrial dysfunction and activates the JNK/Mff signaling pathway, thereby contributing to endothelial dysfunction. Moreover, melatonin inhibited JNK/Mff signaling and sustained ER homeostasis and mitochondrial function, thereby protecting endothelial cells against ox-LDL-induced damage.

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Section: Mitochondrial Membrane Potential (Mmp) Assessmentmentioning

confidence: 99%

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Xie¹,

Zhong

Guo

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…It was reported that 5% of the confirmed cases was in need of intensive care during the COVID-19 outbreak [21]. Renal impairment was found in 63% of the COVID-19 cases in one ongoing case study [22], which may contribute to multiple organ failure and death [23]. As the situation of the current pandemic evolves, extracorporeal organ support readiness has become a crucial part of care delivery [24].…”

Section: Discussion/conclusionmentioning

confidence: 99%

Infection Control Precautions and Care Delivery in Hemodialysis Unit during Coronavirus Disease 2019 Outbreak: A Case Series

Hu¹,

Fu²,

Fan³

et al. 2020

Blood Purif

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Background: With an estimated basic reproductive number of 3.77, the Coronavirus Disease 2019 (COVID-19) continues to spread. It is urgent to exert adequate efforts for the management of dialysis patients, caregivers, and healthcare personnel (HCP). This study aimed at reporting practical workflow, identification of high-risk or suspected cases of COVID-19, and subsequent response measures. Methods: At the time of the COVID-19 outbreak, precautions and practice protocols were applied in our dialysis units (DUs). This single-center study retrospectively reviewed all high-risk/suspected cases from January 23, 2020, to February 10, 2020. Epidemiological, clinical feature, and detailed data on all cases were recorded. Results: Practical workflow for the clinical management of dialysis patients, caregivers, and HCP was initiated. A total of 6 high-risk/suspected cases were identified. Female gender, older age, presence of cardiovascular disease, diabetes, anuresis, immunocompromised status, hypoalbuminemia, and underweight were noticeable features in these cases. Direct evidence of infection or epidemiological risk was detected in five cases. Close monitoring for temperature and oxygen saturation during hemodialysis sessions may be reasonable. No confirmed COVID-19 cases were reported in our DU, but certain cases showed rapid deterioration due to other critically severe condition needing hospitalization. Portable dialysis machines are of great need to ensure dialysis care provision. Conclusions: Our study described a practical workflow for patient-centered management during COVID-19 outbreak. Potential risk factors and underlying clinical patterns were reported. Further studies regarding the efficacy of infection control precautions and practice protocols tailored for dialysis settings are warranted.

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“…The mitochondrial NTT-MMP-2 isoform was also evaluated in acute kidney injury , a frequent complication in severely ill patients that may progress to chronic kidney disease . Mitochondria dysfunction increases oxidative stress and cause tubular inflammation, one of the major fibrotic processes in renal diseases ( Maekawa and Inagi, 2019 ; Husain-Syed et al, 2020 ). Wild-type mice and transgenic NTT-MMP-2 mice were submitted to 40 min of unilateral renal IRI, and the contralateral non-clamped kidney was evaluated for systemic inflammatory responses ( Ceron et al, 2017 ).…”

Section: Ntt-mmp-2 and Renal Dysfunction And Kidney Diseasesmentioning

confidence: 99%

Epigenetic Regulation of the N-Terminal Truncated Isoform of Matrix Metalloproteinase-2 (NTT-MMP-2) and Its Presence in Renal and Cardiac Diseases

et al. 2021

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Several clinical and experimental studies have documented a compelling and critical role for the full-length matrix metalloproteinase-2 (FL-MMP-2) in ischemic renal injury, progressive renal fibrosis, and diabetic nephropathy. A novel N-terminal truncated isoform of MMP-2 (NTT-MMP-2) was recently discovered, which is induced by hypoxia and oxidative stress by the activation of a latent promoter located in the first intron of the MMP2 gene. This NTT-MMP-2 isoform is enzymatically active but remains intracellular in or near the mitochondria. In this perspective article, we first present the findings about the discovery of the NTT-MMP-2 isoform, and its functional and structural differences as compared with the FL-MMP-2 isoform. Based on publicly available epigenomics data from the Encyclopedia of DNA Elements (ENCODE) project, we provide insights into the epigenetic regulation of the latent promoter located in the first intron of the MMP2 gene, which support the activation of the NTT-MMP-2 isoform. We then focus on its functional assessment by covering the alterations found in the kidney of transgenic mice expressing the NTT-MMP-2 isoform. Next, we highlight recent findings regarding the presence of the NTT-MMP-2 isoform in renal dysfunction, in kidney and cardiac diseases, including damage observed in aging, acute ischemia-reperfusion injury (IRI), chronic kidney disease, diabetic nephropathy, and human renal transplants with delayed graft function. Finally, we briefly discuss how our insights may guide further experimental and clinical studies that are needed to elucidate the underlying mechanisms and the role of the NTT-MMP-2 isoform in renal dysfunction, which may help to establish it as a potential therapeutic target in kidney diseases.

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Distant organ dysfunction in acute kidney injury

Cited by 33 publications

References 100 publications

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Infection Control Precautions and Care Delivery in Hemodialysis Unit during Coronavirus Disease 2019 Outbreak: A Case Series

Epigenetic Regulation of the N-Terminal Truncated Isoform of Matrix Metalloproteinase-2 (NTT-MMP-2) and Its Presence in Renal and Cardiac Diseases

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