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• W3100534589 abstract "ABSTRACT The association between reduced myofilament force-generating capacity (F max ) and heart failure (HF) is clear, however the underlying molecular mechanisms are poorly understood. Here, we show the F max decrease arises from impaired BAG3-mediated sarcomere turnover. Myofilament BAG3 decreased in human HF and predicted the extent of F max decrease. This relationship was confirmed using BAG3 +/- mice, which had reduced F max and increased myofilament ubiquitination, suggesting impaired protein turnover. We show cardiac BAG3 operates via the chaperone-assisted selective autophagy complex (CASA), conserved from skeletal muscle, and confirm sarcomeric CASA localization is BAG3/proteotoxic stress-dependent. To determine if increasing BAG3 expression in HF would restore sarcomere proteostasis/F max , HF mice were treated with AAV9/BAG3. Gene therapy fully restored F max after four weeks and decreased ubiquitination. Using mass spectrometry, we identified several sarcomere proteins with increased ubiquitination in HF and four that decreased with AAV9/BAG3. Our findings indicate BAG3-mediated sarcomere turnover is required for myofilament functional maintenance." @default.
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• W3100534589 date "2020-04-12" @default.
• W3100534589 modified "2023-10-18" @default.
• W3100534589 title "Cardiomyocyte Contractile Impairment in Heart Failure Results from Reduced BAG3-mediated Sarcomeric Protein Turnover" @default.
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• W3100534589 doi "https://doi.org/10.1101/2020.04.10.022319" @default.
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