Endothelial factors in the pathogenesis and treatment of chronic kidney disease Part I

Rossi, Gian Paolo; Seccia, Teresa Maria; Barton, Matthias; Danser, A.H. Jan; Leeuw, Peter W. de; Dhaun, Neeraj; Rizzoni, Damiano; Rossignol, Patrick; Ruilope, Luís M.; Meiracker, Anton H. van den; Ito, Sadayoshi; Hasebe, Naoyuki; Webb, David J.

doi:10.1097/hjh.0000000000001599

Cited by 23 publications

(5 citation statements)

References 121 publications

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“…CKD is one of the top public health problems and leading diseases for all-cause mortality globally (Xie et al, 2018). The putative mechanisms regarding the pathogenesis and progression of CKD have been well documented previously (Fogo, 2007; Malyszko, 2010; Eddy et al, 2012; Yang et al, 2017; Cheung et al, 2018; Mihai et al, 2018; Moradi and Vaziri, 2018; Rossi et al, 2018). Briefly, both generic factor-caused genital abnormality of renal development, and other factors (e.g., inflammation, hypertension, diabetes, dyslipidemia, disorder of cytokines and growth factors, proteinuria, podocyte loss, etc.)…”

Section: Preclinical Studies Of the Treatment Of Renal Dysfunction Bymentioning

confidence: 77%

Inhibition of Soluble Epoxide Hydrolase for Renal Health

Liu

2019

Front. Pharmacol.

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A soluble epoxide hydrolase (sEH) mediates the metabolism of epoxy fatty acids to form the corresponding vicinal diols, which are usually inactive or less active than the epoxide substrates. The sEH enzyme presents in many organs, including but not limited to the liver, heart, spleen, lung, and kidney. Here we summarized the changes in the expression and activity of sEH in multiple renal diseases, such as acute kidney injury (AKI), diabetic nephrology (DN), chronic kidney diseases (CKD), hypertension-mediated renal damage, and other renal dysfunctions. We also discussed the pharmacologic effects and the underlying mechanisms of sEH inhibition by using an inhibitor of sEH and/or the generic deletion of sEH on multiple renal diseases. We believe that sEH is a potential therapeutic target for renal dysfunction although the target disease needs further investigation.

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Section: Preclinical Studies Of the Treatment Of Renal Dysfunction Bymentioning

confidence: 77%

Inhibition of Soluble Epoxide Hydrolase for Renal Health

Liu

2019

Front. Pharmacol.

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“…Furthermore, observational studies associate sleep duration with markers of endothelial dysfunction 43 . Thus, given that derangements in the renin-angiotensin-aldosterone system and endothelial dysfunction 44 are well-established mechanisms underlying kidney damage, studies should examine their potential role in the observed association between sleep and CKD to determine the nature of this relation.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Allostatic Load as a Mediator of Sleep and Kidney Outcomes in Black Americans

Lunyera

Davenport

Jackson

et al. 2019

Kidney International Reports

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Introduction Poor sleep associates with adverse chronic kidney disease (CKD) outcomes yet the biological mechanisms underlying this relation remain unclear. One proposed mechanism is via allostatic load, a cumulative biologic measure of stress. Methods Using data from 5177 Jackson Heart Study participants with sleep measures available, we examined the association of self-reported sleep duration: very short, short, recommended, and long (≤5, 6, 7–8, or ≥9 hours per 24 hours, respectively) and sleep quality (high, moderate, low) with prevalent baseline CKD, and estimated glomerular filtration rate (eGFR) decline and incident CKD at follow-up. CKD was defined as eGFR <60 ml/min per 1.73 m 2 or urine albumin-to-creatinine ratio ≥30 mg/g. Models were adjusted for demographics, comorbidities, and kidney function. We further evaluated allostatic load (quantified at baseline using 11 biomarkers from neuroendocrine, metabolic, autonomic, and immune domains) as a mediator of these relations using a process analysis approach. Results Participants with very short sleep duration (vs. 7–8 hours) had greater odds of prevalent CKD (odds ratio [OR] 1.31, 95% confidence interval [CI] 1.03–1.66). Very short, short, or long sleep duration (vs. 7–8 hours) was not associated with kidney outcomes over a median follow-up of 8 years. Low sleep quality (vs. high) associated with greater odds of prevalent CKD (OR 1.26, 95% CI 1.00–1.60) and 0.18 ml/min per 1.73 m 2 (95% CI 0.00–0.36) faster eGFR decline per year. Allostatic load did not mediate the associations of sleep duration or sleep quality with kidney outcomes. Conclusions Very short sleep duration and low sleep quality were associated with adverse kidney outcomes in this all-black cohort, but allostatic load did not appear to mediate these associations.

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“…The physiological role of the ET system in the kidney (Figure 3) appears to be dominated by the high expression of ET B Rs primarily, but not exclusively, located in the principal cells within the inner medullary collecting duct (reviewed in [28][29][30] ). In fact, high-salt diets are powerful stimulators of ET-1 production within the kidney tubule and even nonrenal sources of ET-1.…”

Section: Renal Pathophysiological Effects Of Et-1mentioning

confidence: 99%

Endothelin System in Hypertension and Chronic Kidney Disease

Schiffrin,

Pollock

2024

Hypertension

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ET (endothelin) is a powerful vasoconstrictor 21-amino acid peptide present in many tissues, which exerts many physiological functions across the body and participates as a mediator in many pathological conditions. ETs exert their effects through ET A and ET B receptors, which can be blocked by selective receptor antagonists. ETs were shown to play important roles among others, in systemic hypertension, particularly when resistant or difficult to control, and in pulmonary hypertension, atherosclerosis, cardiac hypertrophy, subarachnoid hemorrhage, chronic kidney disease, diabetic cardiovascular disease, scleroderma, some cancers, etc. To date, ET antagonists are only approved for the treatment of primary pulmonary hypertension and recently for IgA nephropathy and used in the treatment of digital ulcers in scleroderma. However, they may soon be approved for the treatment of patients with resistant hypertension and different types of nephropathy. Here, the role of ETs is reviewed with a special emphasis on participation in and treatment of hypertension and chronic kidney disease.

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Endothelial factors in the pathogenesis and treatment of chronic kidney disease Part I

Cited by 23 publications

References 121 publications

Inhibition of Soluble Epoxide Hydrolase for Renal Health

Inhibition of Soluble Epoxide Hydrolase for Renal Health

Evaluation of Allostatic Load as a Mediator of Sleep and Kidney Outcomes in Black Americans

Endothelin System in Hypertension and Chronic Kidney Disease

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