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ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure

Karoline B Rypdal1,2,3, A Olav Melleby4,5, Emma L Robinson6

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ADAMTSL3 protein protects the heart by regulating transforming growth factor-beta (TGFβ) signaling. Loss of ADAMTSL3 worsens heart failure, while its presence inhibits harmful fibroblast activation and collagen production.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Fibrosis Research

Background:

  • Heart failure is a leading cause of death, often involving cardiac remodelling due to pressure overload.
  • Transforming growth factor-beta (TGFβ) signaling drives cardiac fibroblast (CFB) activation and fibrosis in failing hearts.
  • Targeting pathological TGFβ signaling presents a therapeutic opportunity for heart failure.

Purpose of the Study:

  • To investigate the role of the secreted glycoprotein ADAMTSL3 in regulating TGFβ signaling within the heart.
  • To determine the impact of ADAMTSL3 on cardiac function and remodelling under pressure overload conditions.

Main Methods:

  • Utilized Adamtsl3 knock-out mouse models subjected to pressure overload via aortic banding.
  • Assessed cardiac function, mortality, TGFβ activity, and cardiac fibroblast activation.
  • Examined the effect of ADAMTSL3 overexpression on cultured cardiac fibroblasts, including TGFβ signaling, differentiation, and collagen synthesis.

Main Results:

  • Adamtsl3 knock-out mice exhibited exacerbated cardiac dysfunction, dilatation, and increased mortality following pressure overload.
  • Hearts from knock-out mice showed elevated TGFβ activity and increased cardiac fibroblast activation.
  • Overexpression of ADAMTSL3 in cultured cardiac fibroblasts suppressed TGFβ signaling, myofibroblast differentiation, and collagen production.

Conclusions:

  • ADAMTSL3 plays a crucial role in regulating cardiac TGFβ activity and cardiac fibroblast phenotype.
  • ADAMTSL3 demonstrates a cardioprotective effect by mitigating pathological cardiac remodelling.
  • These findings suggest ADAMTSL3 as a potential therapeutic target for managing heart failure.