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ECM remodeling in hypertensive heart disease

Journal

JOURNAL OF CLINICAL INVESTIGATION
Volume 117, Issue 3, Pages 568-575

Publisher

AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI31044

Keywords

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Funding

  1. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL049192, R01HL063462] Funding Source: NIH RePORTER
  2. NHLBI NIH HHS [R01 HL049192, R01 HL063462, HL63462, HL49192] Funding Source: Medline

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Hypertensive heart disease (HHD) occurs in patients that clinically have both diastolic and systolic heart failure and will soon become the most common cause of heart failure. Two key aspects of heart failure secondary to HHD are the relatively highly prevalent LV hypertrophy and cardiac fibrosis, caused by changes in the local and systemic neurohormonal environment. The fibrotic state is marked by changes in the balance between MMPs and their inhibitors, which alter the composition of the ECM. Importantly, the fibrotic ECM impairs cardiomyocyte function. Recent research suggests that therapies targeting the expression, synthesis, or activation of the enzymes responsible for ECM homeostasis might represent novel opportunities to modify the natural progression of HHD.

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