Published January 28, 2017 | Version v1
Poster Open

Cardiac compliance is acutely modulated through cGMP-PKG signalling

Description

Increased diastolic stiffness due to titin hypophosphorylation and low protein kinase G (PKG) activity is a hallmark of heart failure with preserved ejection fraction (HFpEF). Acute load sensitivity is a well-known factor of decompensation in HFpEF, which has been mainly ascribed to vascular and systolic stiffening, but other factors may be at play.

We aimed to investigate whether there is a diastolic response to acute volume overload (VO), cardiac stretch-induced compliance (SIC), and to ascertain the potential involvement of cGMP-PKG-signalling in this response in several animal models and in the human heart.

Notes

This work is a result of the project DOCnet (NORTE-01-0145-FEDER-000003), supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF) and is supported by European Structural and Investment Funds (ESIF), under Lisbon Portugal Regional Operational Programme and National Funds through FCT - Foundation for Science and Technology under project POCI-01-0145-FEDER-016385.

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