The protective role of small heat shock proteins in cardiac diseases: key role in atrial fibrillation

Xu Hu, Denise M.S. Van Marion, Marit Wiersma, Deli Zhang, Bianca J.J.M. Brundel

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Atrial fibrillation (AF) is the most common tachyarrhythmia which is associated with increased morbidity and mortality. AF usually progresses from a self-terminating paroxysmal to persistent disease. It has been recognized that AF progression is driven by structural remodeling of cardiomyocytes, which results in electrical and contractile dysfunction of the atria. We recently showed that structural remodeling is rooted in derailment of proteostasis, i.e., homeostasis of protein production, function, and degradation. Since heat shock proteins (HSPs) play an important role in maintaining a healthy proteostasis, the role of HSPs was investigated in AF. It was found that especially small heat shock protein (HSPB) levels get exhausted in atrial tissue of patients with persistent AF and that genetic or pharmacological induction of HSPB protects against cardiomyocyte remodeling in experimental models for AF. In this review, we provide an overview of HSPBs as a potential therapeutic target for normalizing proteostasis and suppressing the substrates for AF progression in experimental and clinical AF and discuss HSP activators as a promising therapy to prevent AF onset and progression.

Original languageEnglish
Pages (from-to)665-674
Number of pages10
JournalCell Stress and Chaperones
Volume22
Issue number4
DOIs
Publication statusPublished - 1 Jul 2017

Cite this

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title = "The protective role of small heat shock proteins in cardiac diseases: key role in atrial fibrillation",
abstract = "Atrial fibrillation (AF) is the most common tachyarrhythmia which is associated with increased morbidity and mortality. AF usually progresses from a self-terminating paroxysmal to persistent disease. It has been recognized that AF progression is driven by structural remodeling of cardiomyocytes, which results in electrical and contractile dysfunction of the atria. We recently showed that structural remodeling is rooted in derailment of proteostasis, i.e., homeostasis of protein production, function, and degradation. Since heat shock proteins (HSPs) play an important role in maintaining a healthy proteostasis, the role of HSPs was investigated in AF. It was found that especially small heat shock protein (HSPB) levels get exhausted in atrial tissue of patients with persistent AF and that genetic or pharmacological induction of HSPB protects against cardiomyocyte remodeling in experimental models for AF. In this review, we provide an overview of HSPBs as a potential therapeutic target for normalizing proteostasis and suppressing the substrates for AF progression in experimental and clinical AF and discuss HSP activators as a promising therapy to prevent AF onset and progression.",
keywords = "Atrial fibrillation, Heat shock protein, Proteostasis, Small HSP (HSPB)",
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The protective role of small heat shock proteins in cardiac diseases : key role in atrial fibrillation. / Hu, Xu; Van Marion, Denise M.S.; Wiersma, Marit; Zhang, Deli; Brundel, Bianca J.J.M.

In: Cell Stress and Chaperones, Vol. 22, No. 4, 01.07.2017, p. 665-674.

Research output: Contribution to journalArticleAcademicpeer-review

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T1 - The protective role of small heat shock proteins in cardiac diseases

T2 - key role in atrial fibrillation

AU - Hu, Xu

AU - Van Marion, Denise M.S.

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AU - Zhang, Deli

AU - Brundel, Bianca J.J.M.

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AB - Atrial fibrillation (AF) is the most common tachyarrhythmia which is associated with increased morbidity and mortality. AF usually progresses from a self-terminating paroxysmal to persistent disease. It has been recognized that AF progression is driven by structural remodeling of cardiomyocytes, which results in electrical and contractile dysfunction of the atria. We recently showed that structural remodeling is rooted in derailment of proteostasis, i.e., homeostasis of protein production, function, and degradation. Since heat shock proteins (HSPs) play an important role in maintaining a healthy proteostasis, the role of HSPs was investigated in AF. It was found that especially small heat shock protein (HSPB) levels get exhausted in atrial tissue of patients with persistent AF and that genetic or pharmacological induction of HSPB protects against cardiomyocyte remodeling in experimental models for AF. In this review, we provide an overview of HSPBs as a potential therapeutic target for normalizing proteostasis and suppressing the substrates for AF progression in experimental and clinical AF and discuss HSP activators as a promising therapy to prevent AF onset and progression.

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