Promyelocytic leukemia protein: An atherosclerosis suppressor protein?

Cali B. Corbett; Amanda K. St. Paul; Michael V. Autieri

doi:10.1042/CS20210314

Promyelocytic leukemia protein: An atherosclerosis suppressor protein?

Cali B. Corbett, Amanda K. St. Paul, Michael V. Autieri

Temple University

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

1 Scopus citations

Abstract

As many as 70% of cells in atherosclerotic plaque are vascular smooth muscle cell (VSMC) in origin, and pathways and proteins which regulate VSMC migration, proliferation, and phenotype modulation represent novel targets for rational drug design to reduce atherosclerotic vascular disease. In this volume of Clinical Science, Karle et al. demonstrate that tumor suppressor, promyelocytic leukemia protein (PML) plays an important role in regulation of VSMC phenotype and response to inflammatory stimuli (Clin Sci (2021) 135(7), 887-905; DOI: 10.1042/CS20201399). This important work demonstrates that PML, previously unrecognized as a participant in development of atherosclerosis, may represent a novel target for anti-atherosclerotic therapeutic modalities.

Original language	English
Pages (from-to)	1557-1561
Number of pages	5
Journal	Clinical Science
Volume	135
Issue number	13
DOIs	https://doi.org/10.1042/CS20210314
State	Published - Jul 2021

Keywords

Atherosclerosis/genetics
Humans
Muscle, Smooth, Vascular
Myocytes, Smooth Muscle
Plaque, Atherosclerotic
Promyelocytic Leukemia Protein/genetics

Access to Document

10.1042/CS20210314

Cite this

@article{dc55b8fb60e24788be09c22882c85c6c,

title = "Promyelocytic leukemia protein: An atherosclerosis suppressor protein?",

abstract = "As many as 70% of cells in atherosclerotic plaque are vascular smooth muscle cell (VSMC) in origin, and pathways and proteins which regulate VSMC migration, proliferation, and phenotype modulation represent novel targets for rational drug design to reduce atherosclerotic vascular disease. In this volume of Clinical Science, Karle et al. demonstrate that tumor suppressor, promyelocytic leukemia protein (PML) plays an important role in regulation of VSMC phenotype and response to inflammatory stimuli (Clin Sci (2021) 135(7), 887-905; DOI: 10.1042/CS20201399). This important work demonstrates that PML, previously unrecognized as a participant in development of atherosclerosis, may represent a novel target for anti-atherosclerotic therapeutic modalities.",

keywords = "Atherosclerosis/genetics, Humans, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Plaque, Atherosclerotic, Promyelocytic Leukemia Protein/genetics",

author = "Corbett, {Cali B.} and {St. Paul}, {Amanda K.} and Autieri, {Michael V.}",

note = "{\textcopyright} 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.",

year = "2021",

month = jul,

doi = "10.1042/CS20210314",

language = "English",

volume = "135",

pages = "1557--1561",

journal = "Clinical Science",

issn = "0143-5221",

publisher = "Portland Press Ltd",

number = "13",

}

TY - JOUR

T1 - Promyelocytic leukemia protein

T2 - An atherosclerosis suppressor protein?

AU - Corbett, Cali B.

AU - St. Paul, Amanda K.

AU - Autieri, Michael V.

PY - 2021/7

Y1 - 2021/7

N2 - As many as 70% of cells in atherosclerotic plaque are vascular smooth muscle cell (VSMC) in origin, and pathways and proteins which regulate VSMC migration, proliferation, and phenotype modulation represent novel targets for rational drug design to reduce atherosclerotic vascular disease. In this volume of Clinical Science, Karle et al. demonstrate that tumor suppressor, promyelocytic leukemia protein (PML) plays an important role in regulation of VSMC phenotype and response to inflammatory stimuli (Clin Sci (2021) 135(7), 887-905; DOI: 10.1042/CS20201399). This important work demonstrates that PML, previously unrecognized as a participant in development of atherosclerosis, may represent a novel target for anti-atherosclerotic therapeutic modalities.

AB - As many as 70% of cells in atherosclerotic plaque are vascular smooth muscle cell (VSMC) in origin, and pathways and proteins which regulate VSMC migration, proliferation, and phenotype modulation represent novel targets for rational drug design to reduce atherosclerotic vascular disease. In this volume of Clinical Science, Karle et al. demonstrate that tumor suppressor, promyelocytic leukemia protein (PML) plays an important role in regulation of VSMC phenotype and response to inflammatory stimuli (Clin Sci (2021) 135(7), 887-905; DOI: 10.1042/CS20201399). This important work demonstrates that PML, previously unrecognized as a participant in development of atherosclerosis, may represent a novel target for anti-atherosclerotic therapeutic modalities.

KW - Atherosclerosis/genetics

KW - Humans

KW - Muscle, Smooth, Vascular

KW - Myocytes, Smooth Muscle

KW - Plaque, Atherosclerotic

KW - Promyelocytic Leukemia Protein/genetics

UR - http://www.scopus.com/inward/record.url?scp=85109445498&partnerID=8YFLogxK

UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=purepublist2023&SrcAuth=WosAPI&KeyUT=WOS:000683546000002&DestLinkType=FullRecord&DestApp=WOS

U2 - 10.1042/CS20210314

DO - 10.1042/CS20210314

M3 - Article

C2 - 34192313

SN - 0143-5221

VL - 135

SP - 1557

EP - 1561

JO - Clinical Science

JF - Clinical Science

IS - 13

ER -

Promyelocytic leukemia protein: An atherosclerosis suppressor protein?

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this