Cardiomyocyte-specific ablation of CD36 accelerates the progression from compensated cardiac hypertrophy to heart failure.
about
Nox4 reprograms cardiac substrate metabolism via protein O-GlcNAcylation to enhance stress adaptation.Glucose is preferentially utilized for biomass synthesis in pressure-overloaded hearts: Evidence from fatty acid binding protein-4 and -5 knockout mice.Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart.Statistical considerations in reporting cardiovascular researchMyocardial fatty acid uptake through CD36 is indispensable for sufficient bioenergetic metabolism to prevent progression of pressure overload-induced heart failure
P2860
Cardiomyocyte-specific ablation of CD36 accelerates the progression from compensated cardiac hypertrophy to heart failure.
description
2017 nî lūn-bûn
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2017年の論文
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2017年論文
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2017年論文
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2017年論文
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2017年論文
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2017年論文
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2017年论文
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2017年论文
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2017年论文
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name
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@en
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@nl
type
label
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@en
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@nl
prefLabel
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@en
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@nl
P2093
P2860
P1476
Cardiomyocyte-specific ablatio ...... hypertrophy to heart failure.
@en
P2093
Grant Masson
Jamie J Boisvenue
Jason R B Dyck
Jody Levasseur
Maria Febbraio
Miranda M Sung
Nikole J Byrne
P2860
P304
P356
10.1152/AJPHEART.00626.2016
P577
2017-01-06T00:00:00Z