What question did this study set out to answer?

Determine the in vivo role of muscle ring finger-1 (MuRF1) in mediating cardiac atrophy and the regression of pathological cardiac hypertrophy.

January 24, 2009AJP Heart and Circulatory PhysiologyOpen Access

Muscle ring finger 1 mediates cardiac atrophy in vivo

Q: What does this research mean for the field?

Muscle ring finger-1 (MuRF1) is essential for mediating cardiac atrophy in vivo, including during the therapeutic regression of cardiac hypertrophy and dexamethasone-induced atrophy. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

View Full Paper

Ask AI

Bookmark

Why the study?

Does MuRF1 knockout prevent cardiac atrophy in mouse models of transaortic constriction reversal and dexamethasone-induced atrophy?

Key Points

Determine the in vivo role of muscle ring finger-1 (MuRF1) in mediating cardiac atrophy and the regression of pathological cardiac hypertrophy.
Examined cardiac MuRF1 expression in patients undergoing therapeutic cardiac unloading after left ventricular assist device (LVAD) placement.
Evaluated cardiac mass, cardiomyocyte cross-sectional area, and fetal gene expression in wild-type and MuRF1(-/-) mice following reversal of transaortic constriction (TAC).
Assessed cardiac atrophy response to dexamethasone administration in wild-type and MuRF1(-/-) mice using echocardiography.
Following TAC release, MuRF1(-/-) mice exhibited approximately 70% less reduction in cardiac mass and cardiomyocyte cross-sectional area over 4 weeks compared to wild-type mice, which normalized within 4 days.
Transcriptional down-regulation of hypertrophy markers (beta-myosin heavy chain, smooth muscle actin, brain natriuretic peptide) occurred similarly in both MuRF1(-/-) and wild-type hearts after TAC release.
MuRF1(-/-) mice displayed resistance to dexamethasone-induced cardiac atrophy as measured by echocardiographic analysis.

Structured PICO

Does MuRF1 knockout prevent cardiac atrophy in mouse models of transaortic constriction reversal and dexamethasone-induced atrophy?

Population

Patients after left ventricular assist device placement, and two mouse models: MuRF1(-/-) and wild-type mice undergoing transaortic constriction (TAC) reversal or dexamethasone-induced atrophy

Intervention

MuRF1 gene knockout (MuRF1(-/-))

Comparator

Wild-type mice

Outcome

Cardiac mass and cardiomyocyte cross-sectional areassurrogate

MuRF1 is essential for cardiac atrophy in vivo, both in the setting of therapeutic regression of cardiac hypertrophy and dexamethasone-induced atrophy.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

MuRF1 may be a target to modulate atrophy; animal findings leave open human translation and trials.

Cite This Study

Willis et al. (2009) studied this question.

synapsesocial.com/papers/6a194c8a5d70402e70d9426d https://doi.org/10.1152/ajpheart.00660.2008

Topics

Mechanical circulatory support

View Full Paper

Ask AI

Bookmark