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Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy

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Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy. / Law, Jonathan P.; Price, Anna M.; Pickup, Luke; Radhakrishnan, Ashwin; Weston, Chris; Jones, Alan M.; McGettrick, Helen M.; Chua, Winnie; Steeds, Richard P.; Fabritz, Larissa; Kirchhof, Paulus; Pavlovic, Davor; Townend, Jonathan N.; Ferro, Charles J.

In: J AM HEART ASSOC, Vol. 9, No. 7, e016041, 09.04.2020.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Law, JP, Price, AM, Pickup, L, Radhakrishnan, A, Weston, C, Jones, AM, McGettrick, HM, Chua, W, Steeds, RP, Fabritz, L, Kirchhof, P, Pavlovic, D, Townend, JN & Ferro, CJ 2020, 'Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy', J AM HEART ASSOC, vol. 9, no. 7, e016041. https://doi.org/10.1161/JAHA.120.016041

APA

Law, J. P., Price, A. M., Pickup, L., Radhakrishnan, A., Weston, C., Jones, A. M., McGettrick, H. M., Chua, W., Steeds, R. P., Fabritz, L., Kirchhof, P., Pavlovic, D., Townend, J. N., & Ferro, C. J. (2020). Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy. J AM HEART ASSOC, 9(7), [e016041]. https://doi.org/10.1161/JAHA.120.016041

Vancouver

Law JP, Price AM, Pickup L, Radhakrishnan A, Weston C, Jones AM et al. Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy. J AM HEART ASSOC. 2020 Apr 9;9(7). e016041. https://doi.org/10.1161/JAHA.120.016041

Bibtex

@article{e2a299b96c6f4cd1a51e31e571a79dc8,
title = "Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy",
abstract = "Chronic kidney disease is highly prevalent, affecting 10% to 15% of the adult population worldwide and is associated with increased cardiovascular morbidity and mortality. As chronic kidney disease worsens, a unique cardiovascular phenotype develops characterized by heart muscle disease, increased arterial stiffness, atherosclerosis, and hypertension. Cardiovascular risk is multifaceted, but most cardiovascular deaths in patients with advanced chronic kidney disease are caused by heart failure and sudden cardiac death. While the exact drivers of these deaths are unknown, they are believed to be caused by uremic cardiomyopathy: a specific pattern of myocardial hypertrophy, fibrosis, with both diastolic and systolic dysfunction. Although the pathogenesis of uremic cardiomyopathy is likely to be multifactorial, accumulating evidence suggests increased production of fibroblast growth factor-23 and αKlotho deficiency as potential major drivers of cardiac remodeling in patients with uremic cardiomyopathy. In this article we review the increasing understanding of the physiology and clinical aspects of uremic cardiomyopathy and the rapidly increasing knowledge of the biology of both fibroblast growth factor-23 and αKlotho. Finally, we discuss how dissection of these pathological processes is aiding the development of therapeutic options, including small molecules and antibodies, directly aimed at improving the cardiovascular outcomes of patients with chronic kidney disease and end-stage renal disease.",
keywords = "Cardiorenal syndrome, FGF23, Fibroblast growth factor, Growth factor, Kidney, Treatment, αKlotho",
author = "Law, {Jonathan P.} and Price, {Anna M.} and Luke Pickup and Ashwin Radhakrishnan and Chris Weston and Jones, {Alan M.} and McGettrick, {Helen M.} and Winnie Chua and Steeds, {Richard P.} and Larissa Fabritz and Paulus Kirchhof and Davor Pavlovic and Townend, {Jonathan N.} and Ferro, {Charles J.}",
note = "Publisher Copyright: {\textcopyright} 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.",
year = "2020",
month = apr,
day = "9",
doi = "10.1161/JAHA.120.016041",
language = "English",
volume = "9",
journal = "J AM HEART ASSOC",
issn = "2047-9980",
publisher = "Wiley-Blackwell",
number = "7",

}

RIS

TY - JOUR

T1 - Clinical potential of targeting fibroblast growth factor-23 and αklotho in the treatment of uremic cardiomyopathy

AU - Law, Jonathan P.

AU - Price, Anna M.

AU - Pickup, Luke

AU - Radhakrishnan, Ashwin

AU - Weston, Chris

AU - Jones, Alan M.

AU - McGettrick, Helen M.

AU - Chua, Winnie

AU - Steeds, Richard P.

AU - Fabritz, Larissa

AU - Kirchhof, Paulus

AU - Pavlovic, Davor

AU - Townend, Jonathan N.

AU - Ferro, Charles J.

N1 - Publisher Copyright: © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

PY - 2020/4/9

Y1 - 2020/4/9

N2 - Chronic kidney disease is highly prevalent, affecting 10% to 15% of the adult population worldwide and is associated with increased cardiovascular morbidity and mortality. As chronic kidney disease worsens, a unique cardiovascular phenotype develops characterized by heart muscle disease, increased arterial stiffness, atherosclerosis, and hypertension. Cardiovascular risk is multifaceted, but most cardiovascular deaths in patients with advanced chronic kidney disease are caused by heart failure and sudden cardiac death. While the exact drivers of these deaths are unknown, they are believed to be caused by uremic cardiomyopathy: a specific pattern of myocardial hypertrophy, fibrosis, with both diastolic and systolic dysfunction. Although the pathogenesis of uremic cardiomyopathy is likely to be multifactorial, accumulating evidence suggests increased production of fibroblast growth factor-23 and αKlotho deficiency as potential major drivers of cardiac remodeling in patients with uremic cardiomyopathy. In this article we review the increasing understanding of the physiology and clinical aspects of uremic cardiomyopathy and the rapidly increasing knowledge of the biology of both fibroblast growth factor-23 and αKlotho. Finally, we discuss how dissection of these pathological processes is aiding the development of therapeutic options, including small molecules and antibodies, directly aimed at improving the cardiovascular outcomes of patients with chronic kidney disease and end-stage renal disease.

AB - Chronic kidney disease is highly prevalent, affecting 10% to 15% of the adult population worldwide and is associated with increased cardiovascular morbidity and mortality. As chronic kidney disease worsens, a unique cardiovascular phenotype develops characterized by heart muscle disease, increased arterial stiffness, atherosclerosis, and hypertension. Cardiovascular risk is multifaceted, but most cardiovascular deaths in patients with advanced chronic kidney disease are caused by heart failure and sudden cardiac death. While the exact drivers of these deaths are unknown, they are believed to be caused by uremic cardiomyopathy: a specific pattern of myocardial hypertrophy, fibrosis, with both diastolic and systolic dysfunction. Although the pathogenesis of uremic cardiomyopathy is likely to be multifactorial, accumulating evidence suggests increased production of fibroblast growth factor-23 and αKlotho deficiency as potential major drivers of cardiac remodeling in patients with uremic cardiomyopathy. In this article we review the increasing understanding of the physiology and clinical aspects of uremic cardiomyopathy and the rapidly increasing knowledge of the biology of both fibroblast growth factor-23 and αKlotho. Finally, we discuss how dissection of these pathological processes is aiding the development of therapeutic options, including small molecules and antibodies, directly aimed at improving the cardiovascular outcomes of patients with chronic kidney disease and end-stage renal disease.

KW - Cardiorenal syndrome

KW - FGF23

KW - Fibroblast growth factor

KW - Growth factor

KW - Kidney

KW - Treatment

KW - αKlotho

UR - http://www.scopus.com/inward/record.url?scp=85082496456&partnerID=8YFLogxK

U2 - 10.1161/JAHA.120.016041

DO - 10.1161/JAHA.120.016041

M3 - SCORING: Review article

C2 - 32212912

AN - SCOPUS:85082496456

VL - 9

JO - J AM HEART ASSOC

JF - J AM HEART ASSOC

SN - 2047-9980

IS - 7

M1 - e016041

ER -