PPAR-γ agonists in polycystic kidney disease with frequent development of cardiovascular disorders

Shizuko Nagao, Tamio Yamaguchi

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the monogenic disorders and is characterized by bilateral renal cysts; cysts in other organs including liver, pancreas, spleen, testis and ovary; vascular abnormalities including intracranial aneurysms and subarachnoid hemorrhage; and cardiac disorders such as left ventricular hypertrophy (LVH), mitral valve regurgitation, mitral valve prolapse and aortic regurgitation. Autosomal recessive polycystic kidney disease (ARPKD) is an early-onset multisystem disorder characterized by polycysts divided from the renal collecting ducts, congenital hepatic fibrosis, and ductal plate malformation complicated by pulmonary hyperplasia and systemic hypertension. In these polycystic kidney diseases (PKD), progressive enlargement of the cysts results from the aberrant proliferation of tubule epithelial cells and trans-epithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Peroxisome proliferator-activated receptor-γ (PPAR-γ), a member of the liganddependent nuclear receptor superfamily, is expressed in a variety of tissues, including kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. PPAR-γ agonists ameliorate polycystic kidney, polycystic liver and cardiac defects through β-catenin, c-Myc, CFTR, MCP-1, S6, ERK, and TGF-β signaling pathways in animal models of PKD. In this review, we describe the possible therapeutic value of PPAR-γ agonists in the treatment of renal and hepatic manifestations, and cardiac defects in progressive PKD.

Original languageEnglish
Pages (from-to)292-300
Number of pages9
JournalCurrent Molecular Pharmacology
Volume5
Issue number2
DOIs
Publication statusPublished - 01-01-2012

Fingerprint

Polycystic Kidney Diseases
Peroxisome Proliferator-Activated Receptors
Kidney
Cysts
Liver
Mitral Valve Insufficiency
Fibrosis
Autosomal Recessive Polycystic Kidney
Autosomal Dominant Polycystic Kidney
Fluids and Secretions
S 6
Catenins
Mitral Valve Prolapse
Aortic Valve Insufficiency
Nephrons
Intracranial Aneurysm
Left Ventricular Hypertrophy
Subarachnoid Hemorrhage
Cytoplasmic and Nuclear Receptors
Hyperplasia

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery

Cite this

@article{659d16062cf24b0b9a58fef0ca62133c,
title = "PPAR-γ agonists in polycystic kidney disease with frequent development of cardiovascular disorders",
abstract = "Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the monogenic disorders and is characterized by bilateral renal cysts; cysts in other organs including liver, pancreas, spleen, testis and ovary; vascular abnormalities including intracranial aneurysms and subarachnoid hemorrhage; and cardiac disorders such as left ventricular hypertrophy (LVH), mitral valve regurgitation, mitral valve prolapse and aortic regurgitation. Autosomal recessive polycystic kidney disease (ARPKD) is an early-onset multisystem disorder characterized by polycysts divided from the renal collecting ducts, congenital hepatic fibrosis, and ductal plate malformation complicated by pulmonary hyperplasia and systemic hypertension. In these polycystic kidney diseases (PKD), progressive enlargement of the cysts results from the aberrant proliferation of tubule epithelial cells and trans-epithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Peroxisome proliferator-activated receptor-γ (PPAR-γ), a member of the liganddependent nuclear receptor superfamily, is expressed in a variety of tissues, including kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. PPAR-γ agonists ameliorate polycystic kidney, polycystic liver and cardiac defects through β-catenin, c-Myc, CFTR, MCP-1, S6, ERK, and TGF-β signaling pathways in animal models of PKD. In this review, we describe the possible therapeutic value of PPAR-γ agonists in the treatment of renal and hepatic manifestations, and cardiac defects in progressive PKD.",
author = "Shizuko Nagao and Tamio Yamaguchi",
year = "2012",
month = "1",
day = "1",
doi = "10.2174/1874467211205020292",
language = "English",
volume = "5",
pages = "292--300",
journal = "Current Molecular Pharmacology",
issn = "1874-4702",
publisher = "Bentham Science Publishers",
number = "2",

}

PPAR-γ agonists in polycystic kidney disease with frequent development of cardiovascular disorders. / Nagao, Shizuko; Yamaguchi, Tamio.

In: Current Molecular Pharmacology, Vol. 5, No. 2, 01.01.2012, p. 292-300.

Research output: Contribution to journalReview article

TY - JOUR

T1 - PPAR-γ agonists in polycystic kidney disease with frequent development of cardiovascular disorders

AU - Nagao, Shizuko

AU - Yamaguchi, Tamio

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the monogenic disorders and is characterized by bilateral renal cysts; cysts in other organs including liver, pancreas, spleen, testis and ovary; vascular abnormalities including intracranial aneurysms and subarachnoid hemorrhage; and cardiac disorders such as left ventricular hypertrophy (LVH), mitral valve regurgitation, mitral valve prolapse and aortic regurgitation. Autosomal recessive polycystic kidney disease (ARPKD) is an early-onset multisystem disorder characterized by polycysts divided from the renal collecting ducts, congenital hepatic fibrosis, and ductal plate malformation complicated by pulmonary hyperplasia and systemic hypertension. In these polycystic kidney diseases (PKD), progressive enlargement of the cysts results from the aberrant proliferation of tubule epithelial cells and trans-epithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Peroxisome proliferator-activated receptor-γ (PPAR-γ), a member of the liganddependent nuclear receptor superfamily, is expressed in a variety of tissues, including kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. PPAR-γ agonists ameliorate polycystic kidney, polycystic liver and cardiac defects through β-catenin, c-Myc, CFTR, MCP-1, S6, ERK, and TGF-β signaling pathways in animal models of PKD. In this review, we describe the possible therapeutic value of PPAR-γ agonists in the treatment of renal and hepatic manifestations, and cardiac defects in progressive PKD.

AB - Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the monogenic disorders and is characterized by bilateral renal cysts; cysts in other organs including liver, pancreas, spleen, testis and ovary; vascular abnormalities including intracranial aneurysms and subarachnoid hemorrhage; and cardiac disorders such as left ventricular hypertrophy (LVH), mitral valve regurgitation, mitral valve prolapse and aortic regurgitation. Autosomal recessive polycystic kidney disease (ARPKD) is an early-onset multisystem disorder characterized by polycysts divided from the renal collecting ducts, congenital hepatic fibrosis, and ductal plate malformation complicated by pulmonary hyperplasia and systemic hypertension. In these polycystic kidney diseases (PKD), progressive enlargement of the cysts results from the aberrant proliferation of tubule epithelial cells and trans-epithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Peroxisome proliferator-activated receptor-γ (PPAR-γ), a member of the liganddependent nuclear receptor superfamily, is expressed in a variety of tissues, including kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. PPAR-γ agonists ameliorate polycystic kidney, polycystic liver and cardiac defects through β-catenin, c-Myc, CFTR, MCP-1, S6, ERK, and TGF-β signaling pathways in animal models of PKD. In this review, we describe the possible therapeutic value of PPAR-γ agonists in the treatment of renal and hepatic manifestations, and cardiac defects in progressive PKD.

UR - http://www.scopus.com/inward/record.url?scp=84861752690&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84861752690&partnerID=8YFLogxK

U2 - 10.2174/1874467211205020292

DO - 10.2174/1874467211205020292

M3 - Review article

C2 - 22122459

AN - SCOPUS:84861752690

VL - 5

SP - 292

EP - 300

JO - Current Molecular Pharmacology

JF - Current Molecular Pharmacology

SN - 1874-4702

IS - 2

ER -