Acute Kidney Injury Results in Long-Term Diastolic Dysfunction That Is Prevented by Histone Deacetylase Inhibition

Soranno, Danielle E.; Kirkbride-Romeo, BS Lara; Wennersten, Sara A.; Ding, Kathy; Cavasin, Maria A.; Baker, Peter R.; Altmann, BA Christopher; Bagchi, Rushita A.; Haefner, Korey R.; Steinkühler, Christian; Montford, John R.; Keith, Brysen; Gist, DO Katja M.; McKinsey, Timothy A.; Faubel, Sarah

doi:10.1016/j.jacbts.2020.11.013

Cited by 19 publications

(46 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In an experimental AKI model, mice developed diastolic dysfunction with reduced EF ( Hu et al, 2017 ). However, other authors have shown more recently that AKI mice develop HF with preserved EF ( Fox et al, 2019 ; Soranno et al, 2021 ). In spite of the differences observed, which are possibly based on the method used to induce renal disease and the time of renal damage progression, renal disease mouse models have clearly shown HF development.…”

Section: Cardiovascular Events and Mortality In Renal Diseasementioning

confidence: 99%

Fibroblast Growth Factor-23-Klotho Axis in Cardiorenal Syndrome: Mediators and Potential Therapeutic Targets

et al. 2021

View full text Add to dashboard Cite

Cardiorenal syndrome (CRS) is a complex disorder that refers to the category of acute or chronic kidney diseases that induce cardiovascular disease, and inversely, acute or chronic heart diseases that provoke kidney dysfunction. There is a close relationship between renal and cardiovascular disease, possibly due to the presence of common risk factors for both diseases. Thus, it is well known that renal diseases are associated with increased risk of developing cardiovascular disease, suffering cardiac events and even mortality, which is aggravated in those patients with end-stage renal disease or who are undergoing dialysis. Recent works have proposed mineral bone disorders (MBD) as the possible link between kidney dysfunction and the development of cardiovascular outcomes. Traditionally, increased serum phosphate levels have been proposed as one of the main factors responsible for cardiovascular damage in kidney patients. However, recent studies have focused on other MBD components such as the elevation of fibroblast growth factor (FGF)-23, a phosphaturic bone-derived hormone, and the decreased expression of the anti-aging factor Klotho in renal patients. It has been shown that increased FGF-23 levels induce cardiac hypertrophy and dysfunction and are associated with increased cardiovascular mortality in renal patients. Decreased Klotho expression occurs as renal function declines. Despite its expression being absent in myocardial tissue, several studies have demonstrated that this antiaging factor plays a cardioprotective role, especially under elevated FGF-23 levels. The present review aims to collect the recent knowledge about the FGF-23-Klotho axis in the connection between kidney and heart, focusing on their specific role as new therapeutic targets in CRS.

show abstract

Section: Cardiovascular Events and Mortality In Renal Diseasementioning

confidence: 99%

Fibroblast Growth Factor-23-Klotho Axis in Cardiorenal Syndrome: Mediators and Potential Therapeutic Targets

et al. 2021

View full text Add to dashboard Cite

show abstract

“…CRS classification is denoted by the principal organ dysfunction by temporal sequence and the relative acuity of each illness [30,31]. AKI may lead to diastolic dysfunction within 72 h, but it can persist up to 12 months after AKI, suggesting that systemic effects during the initial AKI episode are likely contributors to long term cardiovascular disease [1,32]. AKI produces systemic effects that increase inflammation, cardiac dysfunction, and metabolic disorders, such as reducing adenosine 5 -triphosphate (ATP) formation in the heart [32].…”

Section: Cisplatin-induced Aki and The Cardiorenal Associationmentioning

confidence: 99%

“…AKI may lead to diastolic dysfunction within 72 h, but it can persist up to 12 months after AKI, suggesting that systemic effects during the initial AKI episode are likely contributors to long term cardiovascular disease [1,32]. AKI produces systemic effects that increase inflammation, cardiac dysfunction, and metabolic disorders, such as reducing adenosine 5 -triphosphate (ATP) formation in the heart [32]. Cardiotoxic manifestations also include heart failure, angina, acute myocardial infarction, thromboembolic events, autonomic cardiovascular dysfunction, hypertension and hypotension, and severe congestive cardiomyopathy [33].…”

Section: Cisplatin-induced Aki and The Cardiorenal Associationmentioning

confidence: 99%

“…Cardiotoxic manifestations also include heart failure, angina, acute myocardial infarction, thromboembolic events, autonomic cardiovascular dysfunction, hypertension and hypotension, and severe congestive cardiomyopathy [33]. adenosine 5'-triphosphate (ATP) formation in the heart [32]. Cardiotoxic manifestations also include heart failure, angina, acute myocardial infarction, thromboembolic events, autonomic cardiovascular dysfunction, hypertension and hypotension, and severe congestive cardiomyopathy [33].…”

Section: Cisplatin-induced Aki and The Cardiorenal Associationmentioning

confidence: 99%

“…Cisplatin induced AKI triggers a degenerative process of medium thickness vessel walls, thus causing the reduction of the vascular lumen in the long term, which associates with the development of hypertension [34,35]. Cardiovascular morbidity and mortality due to long term dysfunction include the interaction of different mechanisms, such as renin-angiotensin-aldosterone system activation, volume overload, and inflammation [2,32,36]. A recent observational study concluded that patients who recovered from testicular cancer three decades after the treatment did not show an overt or subclinical reduction in systolic function.…”

Section: Cisplatin-induced Aki and The Cardiorenal Associationmentioning

confidence: 99%

See 2 more Smart Citations

Mitochondrial Transplantation: Is It a Feasible Therapy to Prevent the Cardiorenal Side Effects of Cisplatin?

Amador-Martínez

Hernández-Cruz

Jiménez-Uribe

et al. 2021

Future Pharmacology

View full text Add to dashboard Cite

Mitochondrial transplantation (MT) is a new experimental approach that has demonstrated positive results reverting mitochondrial alterations in cardiac and kidney dysfunction mainly mediated by oxidative stress. On the other hand, cisplatin is an effective and widely used antineoplastic drug in treating several cancers; however, cisplatin has notorious side effects in different organs, such as the heart, kidneys, liver, and brain; the kidney being one of the most affected. The genitourinary system is the principal excretion pathway of cisplatin, since it is removed from the blood primarily by glomerular filtration and tubular secretion, and it may cause a sudden reduction in the renal function (acute kidney injury “AKI”), in part, by inducing mitochondrial dysfunction and the consequent oxidative stress in the tubular segment. In addition, AKI may associate with cardiac alterations, as occurs in acute cardiorenal syndrome. Due to the high prevalence of renal and cardiac side effects produced by cisplatin, here we discuss the possible use of MT as a novel therapy that could protect tissues by alleviating mitochondrial dysfunction and reducing reactive oxygen species (ROS) production.

show abstract

Measurement of glomerular filtration rate reveals that subcapsular injection of shear‐thinning hyaluronic acid hydrogels does not impair kidney function in mice

Soranno

Kirkbride-Romeo

Han

et al. 2021

J Biomedical Materials Res

Self Cite

View full text Add to dashboard Cite

The continued development of minimally invasive therapeutic implants, such as injectable hydrogels, necessitates the concurrent advancement of methods to best assess their biocompatibility via functional outcomes in vivo. Biomaterial implants have been studied to treat kidney disease; however, assessment of biocompatibility has been limited to biomarker and histological assessments. Techniques now exist to measure kidney function serially in vivo in murine studies via transcutaneous measurements of glomerular filtration rate (tGFR). In this study, adult male and female wild-type BalbC mice underwent right unilateral nephrectomy. The remaining solitary left kidney was allowed 4 weeks to recover via compensatory hypertrophy, after which subcapsular injection of either saline or shear-thinning hyaluronic acid hydrogel was performed.Serial tGFR measurements before and after treatment were used to assess the effect of hydrogel injection on kidney filtration. Urine and serum biomarkers of kidney function, and kidney histology were also quantified. Hydrogel injection did not affect kidney function, as assessed by tGFR. Results were in agreement with standard metrics of serum and urine biomarkers of injury as well as histological assessment of inflammation. The model developed provides a direct functional assessment of implant compatibility for the treatment of kidney disease and impact on kidney function.

show abstract

Acute Kidney Injury Results in Long-Term Diastolic Dysfunction That Is Prevented by Histone Deacetylase Inhibition

Abstract: Visual Abstract

Cited by 19 publications

References 68 publications

Fibroblast Growth Factor-23-Klotho Axis in Cardiorenal Syndrome: Mediators and Potential Therapeutic Targets

Fibroblast Growth Factor-23-Klotho Axis in Cardiorenal Syndrome: Mediators and Potential Therapeutic Targets

Mitochondrial Transplantation: Is It a Feasible Therapy to Prevent the Cardiorenal Side Effects of Cisplatin?

Measurement of glomerular filtration rate reveals that subcapsular injection of shear‐thinning hyaluronic acid hydrogels does not impair kidney function in mice

Contact Info

Product

Resources

About