Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice

Abstract PIKfyve is an evolutionarily conserved lipid kinase that regulates pleiotropic cellular functions. Here, we identify PIKfyve as a key regulator of cardiometabolic status and mitochondrial integrity in chronic diet‐induced obesity. In vitro, we show that PIKfyve is critical for the control o...

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Main Authors: Helene Tronchere, Mathieu Cinato, Andrei Timotin, Laurie Guitou, Camille Villedieu, Helene Thibault, Delphine Baetz, Bernard Payrastre, Philippe Valet, Angelo Parini, Oksana Kunduzova, Frederic Boal
Format: Article
Language:English
Published: Springer Nature 2017-04-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201607096
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author Helene Tronchere
Mathieu Cinato
Andrei Timotin
Laurie Guitou
Camille Villedieu
Helene Thibault
Delphine Baetz
Bernard Payrastre
Philippe Valet
Angelo Parini
Oksana Kunduzova
Frederic Boal
author_facet Helene Tronchere
Mathieu Cinato
Andrei Timotin
Laurie Guitou
Camille Villedieu
Helene Thibault
Delphine Baetz
Bernard Payrastre
Philippe Valet
Angelo Parini
Oksana Kunduzova
Frederic Boal
author_sort Helene Tronchere
collection DOAJ
description Abstract PIKfyve is an evolutionarily conserved lipid kinase that regulates pleiotropic cellular functions. Here, we identify PIKfyve as a key regulator of cardiometabolic status and mitochondrial integrity in chronic diet‐induced obesity. In vitro, we show that PIKfyve is critical for the control of mitochondrial fragmentation and hypertrophic and apoptotic responses to stress. We also provide evidence that inactivation of PIKfyve by the selective inhibitor STA suppresses excessive mitochondrial ROS production and apoptosis through a SIRT3‐dependent pathway in cardiomyoblasts. In addition, we report that chronic STA treatment improves cardiometabolic profile in a mouse model of cardiomyopathy linked to obesity. We provide evidence that PIKfyve inhibition reverses obesity‐induced cardiac mitochondrial damage and apoptosis by activating SIRT3. Furthermore, treatment of obese mice with STA improves left ventricular function and attenuates cardiac hypertrophy. In contrast, STA is not able to reduce isoproterenol‐induced cardiac hypertrophy in SIRT3.KO mice. Altogether, these results unravel a novel role for PIKfyve in obesity‐associated cardiomyopathy and provide a promising therapeutic strategy to combat cardiometabolic complications in obesity.
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spelling doaj-art-ffde4b6b99b64e4fbcf721fdde0f4a1e2025-08-20T03:06:00ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842017-04-019677078510.15252/emmm.201607096Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese miceHelene Tronchere0Mathieu Cinato1Andrei Timotin2Laurie Guitou3Camille Villedieu4Helene Thibault5Delphine Baetz6Bernard Payrastre7Philippe Valet8Angelo Parini9Oksana Kunduzova10Frederic Boal11INSERM U1048 I2MCINSERM U1048 I2MCINSERM U1048 I2MCINSERM U1048 I2MCCarMeN Laboratory, Inserm U1060, Univ‐Lyon, Université Claude Bernard Lyon 1CarMeN Laboratory, Inserm U1060, Univ‐Lyon, Université Claude Bernard Lyon 1CarMeN Laboratory, Inserm U1060, Univ‐Lyon, Université Claude Bernard Lyon 1INSERM U1048 I2MCINSERM U1048 I2MCINSERM U1048 I2MCINSERM U1048 I2MCINSERM U1048 I2MCAbstract PIKfyve is an evolutionarily conserved lipid kinase that regulates pleiotropic cellular functions. Here, we identify PIKfyve as a key regulator of cardiometabolic status and mitochondrial integrity in chronic diet‐induced obesity. In vitro, we show that PIKfyve is critical for the control of mitochondrial fragmentation and hypertrophic and apoptotic responses to stress. We also provide evidence that inactivation of PIKfyve by the selective inhibitor STA suppresses excessive mitochondrial ROS production and apoptosis through a SIRT3‐dependent pathway in cardiomyoblasts. In addition, we report that chronic STA treatment improves cardiometabolic profile in a mouse model of cardiomyopathy linked to obesity. We provide evidence that PIKfyve inhibition reverses obesity‐induced cardiac mitochondrial damage and apoptosis by activating SIRT3. Furthermore, treatment of obese mice with STA improves left ventricular function and attenuates cardiac hypertrophy. In contrast, STA is not able to reduce isoproterenol‐induced cardiac hypertrophy in SIRT3.KO mice. Altogether, these results unravel a novel role for PIKfyve in obesity‐associated cardiomyopathy and provide a promising therapeutic strategy to combat cardiometabolic complications in obesity.https://doi.org/10.15252/emmm.201607096apoptosiscardiac hypertrophymitochondriaPIKfyveSIRT3
spellingShingle Helene Tronchere
Mathieu Cinato
Andrei Timotin
Laurie Guitou
Camille Villedieu
Helene Thibault
Delphine Baetz
Bernard Payrastre
Philippe Valet
Angelo Parini
Oksana Kunduzova
Frederic Boal
Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
EMBO Molecular Medicine
apoptosis
cardiac hypertrophy
mitochondria
PIKfyve
SIRT3
title Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
title_full Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
title_fullStr Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
title_full_unstemmed Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
title_short Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice
title_sort inhibition of pikfyve prevents myocardial apoptosis and hypertrophy through activation of sirt3 in obese mice
topic apoptosis
cardiac hypertrophy
mitochondria
PIKfyve
SIRT3
url https://doi.org/10.15252/emmm.201607096
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