Pathological Cardiac Hypertrophy Alters Intracellular Targeting of Phosphodiesterase Type 5 From Nitric Oxide Synthase-3 to Natriuretic Peptide Signaling | Zendy

Manling Zhang | Zendy; Eiki Takimoto | Zendy; Dongik Lee | Zendy; Célio X.C. Santos | Zendy; Taishi Nakamura | Zendy; Steven Hsu | Zendy; Aiyang Jiang | Zendy; Takahiro Nagayama | Zendy; Djahida Bedja | Zendy; Yuan Yuan | Zendy; Philip Eaton | Zendy; Ajay M. Shah | Zendy; David A. Kass | Zendy

Open Access

Pathological Cardiac Hypertrophy Alters Intracellular Targeting of Phosphodiesterase Type 5 From Nitric Oxide Synthase-3 to Natriuretic Peptide Signaling

Author(s) -

Manling Zhang,

Eiki Takimoto,

Dongik Lee,

Célio X.C. Santos,

Taishi Nakamura,

Steven Hsu,

Aiyang Jiang,

Takahiro Nagayama,

Djahida Bedja,

Yuan Yuan,

Philip Eaton,

Ajay M. Shah,

David A. Kass

Publication year - 2012

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.112.090977

Subject(s) - medicine , intracellular , nitric oxide synthase , natriuretic peptide , phosphodiesterase , cardiac hypertrophy , nitric oxide , pathological , atrial natriuretic peptide , endocrinology , muscle hypertrophy , pharmacology , microbiology and biotechnology , enzyme , biochemistry , heart failure , biology

In the normal heart, phosphodiesterase type 5 (PDE5) hydrolyzes cGMP coupled to nitric oxide- (specifically from nitric oxide synthase 3) but not natriuretic peptide (NP)-stimulated guanylyl cyclase. PDE5 is upregulated in hypertrophied and failing hearts and is thought to contribute to their pathophysiology. Because nitric oxide signaling declines whereas NP-derived cGMP rises in such diseases, we hypothesized that PDE5 substrate selectivity is retargeted to blunt NP-derived signaling.

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