Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging

Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodeg...

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Vydáno v:International journal of molecular sciences Ročník 23; číslo 17; s. 10135
Hlavní autoři: Hwang, Hyun Jung, Kim, Nayeon, Herman, Allison B., Gorospe, Myriam, Lee, Jae-Seon
Médium: Journal Article
Jazyk:angličtina
Vydáno: Basel MDPI AG 04.09.2022
MDPI
Témata:
Age
Aging
Apoptosis
Atherosclerosis
Autophagy
Cardiovascular disease
Cell cycle
Chemokines
Coronary vessels
Cyclin-dependent kinases
Cytokines
DNA damage
Endothelium
Enzymes
Hypertension
Kinases
Metabolism
Mitochondria
Nitric oxide
Oxidative stress
Phosphorylation
Physiology
Polyploidy
Proteins
Review
Veins & arteries
ISSN:1422-0067, 1661-6596, 1422-0067
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Abstract Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases.
AbstractList Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases.
Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases.Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases.
Author Hwang, Hyun Jung
Lee, Jae-Seon
Herman, Allison B.
Kim, Nayeon
Gorospe, Myriam
AuthorAffiliation 3 Program in Biomedical Science and Engineering, College of Medicine, Inha University, Incheon 22212, Korea
2 Department of Molecular Medicine, College of Medicine, Inha University, Incheon 22212, Korea
4 Laboratory of Genetics and Genomics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA
1 Research Center for Controlling Intercellular Communication, College of Medicine, Inha University, Incheon 22212, Korea
AuthorAffiliation_xml – name: 1 Research Center for Controlling Intercellular Communication, College of Medicine, Inha University, Incheon 22212, Korea
– name: 3 Program in Biomedical Science and Engineering, College of Medicine, Inha University, Incheon 22212, Korea
– name: 4 Laboratory of Genetics and Genomics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA
– name: 2 Department of Molecular Medicine, College of Medicine, Inha University, Incheon 22212, Korea
Author_xml – sequence: 1
  givenname: Hyun Jung
  surname: Hwang
  fullname: Hwang, Hyun Jung
– sequence: 2
  givenname: Nayeon
  surname: Kim
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– sequence: 3
  givenname: Allison B.
  orcidid: 0000-0003-3826-3247
  surname: Herman
  fullname: Herman, Allison B.
– sequence: 4
  givenname: Myriam
  orcidid: 0000-0001-5439-3434
  surname: Gorospe
  fullname: Gorospe, Myriam
– sequence: 5
  givenname: Jae-Seon
  orcidid: 0000-0001-6002-5267
  surname: Lee
  fullname: Lee, Jae-Seon
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Snippet Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs)...
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SubjectTerms Age
Aging
Apoptosis
Atherosclerosis
Autophagy
Cardiovascular disease
Cell cycle
Chemokines
Coronary vessels
Cyclin-dependent kinases
Cytokines
DNA damage
Endothelium
Enzymes
Hypertension
Kinases
Metabolism
Mitochondria
Nitric oxide
Oxidative stress
Phosphorylation
Physiology
Polyploidy
Proteins
Review
Veins & arteries
Title Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging
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