Beta1-Adrenergic Receptor Cleavage and Regulation by Elastase

Jing Zhu; Susan F. Steinberg

doi:10.1016/j.jacbts.2023.02.002

Beta₁-Adrenergic Receptor Cleavage and Regulation by Elastase

Jing Zhu, Susan F. Steinberg

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

The decrease in β₁-adrenergic receptor responsiveness in heart failure is attributed conventionally to agonist-dependent desensitization. We identify elastase-dependent β₁-adrenergic receptor cleavage as a novel proteolytic mechanism that disrupts β₁-adrenergic receptor responsiveness in the setting of tissue injury or inflammation.

Original language	English (US)
Pages (from-to)	976-988
Number of pages	13
Journal	JACC: Basic to Translational Science
Volume	8
Issue number	8
DOIs	https://doi.org/10.1016/j.jacbts.2023.02.002
State	Published - Aug 2023
Externally published	Yes

Keywords

elastase
glycosylation
proteolysis
β-adrenergic receptor

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

Access to Document

10.1016/j.jacbts.2023.02.002

Cite this

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title = "Beta1-Adrenergic Receptor Cleavage and Regulation by Elastase",

abstract = "The decrease in β1-adrenergic receptor responsiveness in heart failure is attributed conventionally to agonist-dependent desensitization. We identify elastase-dependent β1-adrenergic receptor cleavage as a novel proteolytic mechanism that disrupts β1-adrenergic receptor responsiveness in the setting of tissue injury or inflammation.",

keywords = "elastase, glycosylation, proteolysis, β-adrenergic receptor",

author = "Jing Zhu and Steinberg, {Susan F.}",

note = "Publisher Copyright: {\textcopyright} 2023 The Authors",

year = "2023",

month = aug,

doi = "10.1016/j.jacbts.2023.02.002",

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AU - Steinberg, Susan F.

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AB - The decrease in β1-adrenergic receptor responsiveness in heart failure is attributed conventionally to agonist-dependent desensitization. We identify elastase-dependent β1-adrenergic receptor cleavage as a novel proteolytic mechanism that disrupts β1-adrenergic receptor responsiveness in the setting of tissue injury or inflammation.

KW - elastase

KW - glycosylation

KW - proteolysis

KW - β-adrenergic receptor

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