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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Age-Dependent RGS5 Loss in Pericytes Induces Cardiac Dysfunction and Fibrosis.

Anita Tamiato1,2,3, Lukas S Tombor1,2,3, Ariane Fischer1

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Aging impairs cardiac pericytes, reducing vascular stability. Loss of RGS5 in these cells leads to heart dysfunction and fibrosis, highlighting RGS5

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Cellular and Molecular Medicine

Background:

  • Pericytes are crucial mural cells supporting vascular network stability.
  • Aging is a significant risk factor for cardiovascular diseases, but its impact on cardiac pericytes remains unclear.

Purpose of the Study:

  • To investigate the effects of aging on cardiac pericytes.
  • To elucidate the role of Regulator of G-protein signaling 5 (RGS5) in cardiac pericyte function during aging.

Main Methods:

  • Utilized single-nucleus RNA sequencing and histological analysis in murine models.
  • Performed in vivo and in vitro loss-of-function studies for RGS5.
  • Conducted co-culture experiments with pericytes and fibroblasts.

Main Results:

  • Aging decreased pericyte area and capillary coverage in the heart.
  • Reduced RGS5 expression was observed in aged cardiac pericytes.
  • RGS5 deletion impaired cardiac function, increased fibrosis, and altered pericyte gene expression (e.g., ECM components, TGFB2, PDGFB).
  • RGS5-deficient pericyte supernatant activated fibroblasts via a TGFβ2-dependent pathway.

Conclusions:

  • RGS5 is identified as a critical regulator of cardiac pericyte function in aging.
  • RGS5 deficiency contributes to cardiac dysfunction and myocardial fibrosis, key features of cardiac aging.