What is the clinical evidence from this study?

Population: Cardiac overload and heart failure. Intervention: Hsp22 deletion vs. Wild-type mice. Primary outcome: Transition into heart failure and mortality.

What question did this study set out to answer?

To determine the functional role and mechanistic signaling pathways of H11 kinase/Hsp22 during cardiac pressure overload.

July 12, 2011CirculationOpen Access

H11 Kinase/Heat Shock Protein 22 Deletion Impairs Both Nuclear and Mitochondrial Functions of STAT3 and Accelerates the Transition Into Heart Failure on Cardiac Overload

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Key result

Hsp22 deletion in mice exposed to pressure overload accelerated the transition into heart failure and increased mortality by impairing nuclear and mitochondrial functions of STAT3.

Why the study?

Does Hsp22 deletion accelerate the transition into heart failure in a mouse model of cardiac pressure overload?

Key Points

To determine the functional role and mechanistic signaling pathways of H11 kinase/Hsp22 during cardiac pressure overload.
Generated an Hsp22 knockout mouse model subjected to cardiac pressure overload in vivo.
Evaluated gene expression profiles by microarray, nuclear STAT3 phosphorylation, and mitochondrial respiration alongside STAT3 mitochondrial translocation.
Conducted in vitro gene silencing and overexpression studies in isolated neonatal rat cardiomyocytes to identify upstream regulators of STAT3.
Hsp22 knockout mice exposed to pressure overload developed reduced hypertrophy, greater ventricular dilation, impaired contractile function, increased interstitial collagen, and accelerated transition to heart failure with increased mortality.
Hsp22 deficiency impaired nuclear STAT3 tyrosine phosphorylation and target gene transactivation, mediated by reduced NF-κB-dependent interleukin-6 expression.
Loss of Hsp22 significantly reduced STAT3 translocation into mitochondria and decreased mitochondrial respiration.

Structured PICO

Does Hsp22 deletion accelerate the transition into heart failure in a mouse model of cardiac pressure overload?

Population

Knockout mouse model of Hsp22 deletion and isolated neonatal rat cardiomyocytes

Intervention

Hsp22 deletion (knockout) and exposure to pressure overload

Comparator

Wild-type mice exposed to pressure overload

Outcome

Development of hypertrophy, ventricular dilation, contractile function, transition into heart failure, and mortalitysurrogate

Hsp22 is a novel activator of nuclear and mitochondrial STAT3 functions, and its deletion accelerates heart failure and mortality during pressure overload.

Discussion

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

Implication

No immediate clinical implications from mouse data; leaves open Hsp22-STAT3 as a therapeutic target for future study.

Cite This Study

Qiu et al. (2011) studied Cardiac overload and heart failure. Hsp22 deletion vs. Wild-type mice was evaluated on Transition into heart failure and mortality. Hsp22 deletion in mice exposed to pressure overload accelerated the transition into heart failure and increased mortality by impairing nuclear and mitochondrial functions of STAT3.

synapsesocial.com/papers/6a79f7669092edbae3f38ae6 https://doi.org/10.1161/circulationaha.110.013847

Topics

Heart failure HFrEF treatment

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H11 Kinase/Heat Shock Protein 22 Deletion Impairs Both Nuclear and Mitochondrial Functions of STAT3 and Accelerates the Transition Into Heart Failure on Cardiac Overload

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

H11 Kinase/Heat Shock Protein 22 Deletion Impairs Both Nuclear and Mitochondrial Functions of STAT3 and Accelerates the Transition Into Heart Failure on Cardiac Overload

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

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