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Cardiac Microvascular Endothelial Cells in Pressure Overload-Induced Heart Disease.
Sander Trenson1, Hadewich Hermans1, Sander Craps1
1Department of Cardiovascular Sciences (S.T., H.H., S.C., P.P., J.V.W., H.G., D.V., F.W., E.C., J.A.S., F.R., B. Meuris, B. Meyns, W.O., J.D., K.G., J.-U.V., M.-C.H., P.H., A.L., S.J.), KU Leuven, Belgium.
Circulation. Heart Failure
|January 19, 2021
Summary
Chronic pressure overload alters cardiac microvascular endothelial cells (MiVEC), leading to fibrosis and impaired angiogenesis. These changes, particularly in women, highlight MiVEC as therapeutic targets for heart failure.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Heart Failure Pathophysiology
Background:
- Chronic pressure overload is a known precursor to heart failure.
- The specific role of cardiac microvascular endothelial cells (MiVEC) in this process is not well understood.
- This study investigates the adaptations of MiVEC under pressure overload conditions.
Purpose of the Study:
- To characterize the transcriptional, metabolic, and functional changes in cardiac MiVEC during pressure overload.
- To compare these adaptations in a mouse model and in patients with aortic stenosis (AS).
- To identify potential therapeutic targets within MiVEC.
Main Methods:
- Utilized transverse aortic constriction in Tie2-Gfp mice to induce pressure overload.
- Performed RNA sequencing on isolated cardiac MiVEC.
- Validated findings in MiVEC from AS patients and correlated molecular data with clinical phenotypes.
Main Results:
- Pressure overload led to significant gene expression changes in MiVEC, particularly those involved in matrix regulation.
- MiVEC exhibited increased fatty acid oxidation, proline content, and procollagen secretion.
- Altered MiVEC function resulted in impaired angiogenesis, fibrosis, and worsened diastolic function, notably in female patients.
Conclusions:
- Cardiac MiVEC undergo substantial transcriptional and metabolic reprogramming under pressure overload.
- These MiVEC adaptations contribute to interstitial fibrosis and reduced angiogenesis.
- The molecular alterations in MiVEC are more pronounced in women and represent potential targets for heart failure interventions.
