SS31 therapy effectively protects the heart against transverse aortic constriction-induced hypertrophic cardiomyopathy damage.

In mice with TAC-induced cardiomyopathy, LVEF at day 60 was higher with SS31 than with TAC alone, but still lower than in sham-operated mice.

In plain wordsIn mice with heart damage from aortic constriction, SS31 kept heart pumping higher than no treatment, but not as high as in healthy mice.

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In mice with TAC-induced cardiomyopathy, sarcomere length at day 60 was higher with SS31 than with TAC alone, but still lower than in sham-operated mice.

In plain wordsIn mice with heart damage from aortic constriction, SS31 kept heart muscle units longer than no treatment, but not as long as in healthy mice.

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In mice with TAC-induced cardiomyopathy, the LVEDd/LVESd ratio showed the opposite pattern to LVEF, so it was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, a heart-size measure was lower with SS31 than with no treatment.

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In mice with TAC-induced cardiomyopathy, the ratio of heart weight to tibial length showed the opposite pattern to LVEF, so it was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, heart weight relative to body size was lower with SS31 than with no treatment.

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In mice with TAC-induced cardiomyopathy, the number of apoptotic nuclei in the heart showed the opposite pattern to LVEF, so it was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave fewer dying cell nuclei in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, inflammatory cell biomarkers (CD14+, F4/80+) in the heart were lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower inflammation markers in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, the oxidative-stress biomarker H2DCFDA+ in the heart was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave a lower oxidative-stress marker in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, the disorganized score of the endocardium was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave less disorganized heart lining than no treatment.

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In mice with TAC-induced cardiomyopathy, fibrotic and collagen-deposition areas in the heart were smaller with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave less scar tissue in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of inflammatory proteins (PDGF, TNF-α, NF-κB, COX-2) was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of inflammation proteins in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of oxidative-stress proteins (NOX-1, NOX-2, oxidized protein) was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of oxidative-stress proteins in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of fibrotic proteins (TGF-β, Smad3) was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of scarring proteins in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of apoptotic proteins (cleaved-caspase-3, cleaved-PARP) was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of cell-death proteins in the heart than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of the pressure/volume overload markers BNP and β-MHC was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of heart strain markers than no treatment.

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In mice with TAC-induced cardiomyopathy, CTGF protein expression was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave a lower level of the scarring protein CTGF than no treatment.

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In mice with TAC-induced cardiomyopathy, the mitochondrial-damage marker cytosolic cytochrome-C was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave a lower marker of damage to the energy-producing parts of cells than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of the signaling proteins p-ERK1/2, p-Akt and PI3K was lower with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave lower levels of several cell-signaling proteins than no treatment.

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In mice with TAC-induced cardiomyopathy, expression of the antioxidant proteins HO-1 and Nrf2 was higher with SS31 than with TAC alone.

In plain wordsIn mice with heart damage from aortic constriction, SS31 gave higher levels of antioxidant proteins than no treatment.

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In H9C2 cells, SS31 suppressed angiotensin-II induced protein expression of BNP/β-MHC, ATM, p-P38 and P53.

In plain wordsIn lab-grown heart cells, SS31 lowered several stress and damage proteins that angiotensin-II had raised.

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In H9C2 cells, SS31 suppressed angiotensin-II induced ATP damage.

In plain wordsIn lab-grown heart cells, SS31 lowered the loss of cell energy (ATP) that angiotensin-II had caused.

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In fibroblasts, SS31 suppressed protein expression of pro-collagen-I and CTGF.

In plain wordsIn lab-grown connective-tissue cells (fibroblasts), SS31 lowered levels of scarring proteins.

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