Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
December 7, 1999CirculationOpen Access

Overexpression of SERCA2a induced a faster contraction velocity (26.7+/-6.7% versus 16.6+/-2.7% shortening per second, P<0.005) and enhanced relaxation velocity (32.0+/-10.1% versus 15.1+/-2.4%, P<0.005).

View Full Paper
Ask AI
Bookmark
Share

Why the study?

Does SERCA2a gene transfer improve contractile function in isolated cardiomyocytes from failing human hearts?

Population

Isolated human ventricular myocytes from 10 patients with end-stage heart failure

Comparison

Gene transfer to overexpress SERCA2a vs Failing cardiomyocytes not overexpressing SERCA2a

Design

Preclinical

Authors

FMFederica del MonteSHSiân E. HardingUSUlrich Schmidt

Discussion

Loading...

Member takes

Overview

Supports SERCA2a gene therapy development in heart failure; leaves open translation from animal cardiomyocyte models to patients.

Structured PICO

Does SERCA2a gene transfer improve contractile function in isolated cardiomyocytes from failing human hearts?

P
Population
Isolated human ventricular myocytes from 10 patients with end-stage heart failure
I
Intervention
Gene transfer to overexpress SERCA2a
C
Comparator
Failing cardiomyocytes not overexpressing SERCA2a
O
Outcome
Intracellular Ca(2+) handling and contractile function (contraction velocity, relaxation velocity, diastolic Ca2+, systolic Ca2+)surrogate

SERCA2a gene transfer restores contractile function and calcium handling in failing human cardiomyocytes, providing preclinical support for gene-based therapies in heart failure.

Cite This Study

Monte et al. (1999) studied this question.

synapsesocial.com/papers/6a70387d87f92105712789f2https://doi.org/10.1161/01.cir.100.23.2308
View Full Paper
Ask AI
Bookmark
Share