Key result
Pressure-overload cardiac hypertrophy reduces SERCA2a protein levels by ~44% while increasing calreticulin.
Why the study?
It was unknown whether sarcoplasmic reticulum Ca(2+)-storing proteins, including calsequestrin and calreticulin, are altered during pressure-overload cardiac hypertrophy.
Population
Rats with pressure overload 4 weeks after abdominal aortic constriction (n=7) and sham-operated control rats (n=6)
Comparison
Pressure overload induced by abdominal aortic constriction vs sham operation
Design
Preclinical study with Western blot and immunohistochemical analysis
Follow-up
4 weeks
Authors
Loading...
May link calcium-handling shifts to contractile impairment in hypertrophy; leaves open relevance to human HF therapies.
p-value: p=<0.01
Pressure-overload cardiac hypertrophy alters sarcoplasmic reticulum calcium-storing proteins, specifically decreasing Ca(2+)-ATPase and increasing calreticulin, potentially contributing to contractile dysfunction.
Tsutsui et al. (1997) studied Pressure-overload cardiac hypertrophy (n=13). Abdominal aortic constriction (pressure overload) vs. Sham-operated control was evaluated on Sarcoplasmic reticulum Ca(2+)-ATPase protein level (p=<0.01). Pressure-overload cardiac hypertrophy in rats decreased SR Ca(2+)-ATPase protein levels to 56% of control (P<0.01) and increased calreticulin by 120% (P<0.05).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: