Changes in vascular identity during vascular remodeling

Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venou...

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Published inJVS-vascular science Vol. 6; p. 100282
Main Authors Aoyagi, Yukihiko, Schwartz, Andrew W., Li, Zhuo, Bai, Hualong, Gonzalez, Luis, Lazcano Etchebarne, Cayetana, Ohashi, Yuichi, Kano, Masaki, Ho, Bryan, Martin, Kathleen, Dardik, Alan
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Abstract Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity. This is a review of experimental literature. These proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype. Changes in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases. Vascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions. [Display omitted]
AbstractList Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity.BackgroundVascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity.This is a review of experimental literature.MethodsThis is a review of experimental literature.These proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype.ResultsThese proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype.Changes in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases.ConclusionsChanges in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases.Vascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions.Clinical RelevanceVascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions.
Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity. This is a review of experimental literature. These proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype. Changes in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases. Vascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions.
Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define cellular identity as arteries, veins, and lymphatic vessels: Ephrin-B2 and Notch determine arterial identity, EphB4 and COUP-TFII determine venous identity, and Prox1 determines lymphatic identity. This is a review of experimental literature. These proteins determine identity during development before the first heartbeat. Hemodynamic changes in adulthood can also alter vascular identity. Changes in identity markers coincide with changes in vascular cell phenotype or disease and thus may play a role in regulating both normal and pathological vascular remodeling. Vascular diseases such as arteriovenous malformations and pulmonary hypertension are driven by changes in cell phenotype and vessel identity. Surgical interventions such as arteriovenous fistula (AVF) creation and arterial bypass using vein grafts induce alterations in identity; vein grafts lose their venous identity, but do not acquire arterial identity, whereas venous limbs of AVF gain arterial identity while retaining their venous identity. After patch angioplasty, vascular patches remodel in their environment. Patches in the venous environment acquire venous identity and patches in the arterial environment develop arterial identity. Interestingly, patches in the venous outflow of AVF gain a mixed venous-arterial phenotype. Changes in vascular identity drive vascular remodeling in both physiological and pathological settings, with potential implications for therapeutic strategies targeting vascular diseases. Vascular remodeling is essential for both physiological and pathological vascular adaptation. Changes in vascular identity occur in response to hemodynamic forces and mediate vascular remodeling during development, in disease states, and after surgical and endovascular interventions. Alterations in arterial and venous molecular markers of identity regulate cellular phenotype, the extracellular matrix, and vessel wall structure, ultimately determining long-term vessel function. Understanding the molecular regulatory pathways controlling vascular identity provides insight into understanding the mechanisms of vascular remodeling and may identify potential therapeutic targets to treat vascular disease and improve outcomes after vascular interventions. [Display omitted]
ArticleNumber 100282
Author Aoyagi, Yukihiko
Kano, Masaki
Schwartz, Andrew W.
Li, Zhuo
Gonzalez, Luis
Lazcano Etchebarne, Cayetana
Dardik, Alan
Ohashi, Yuichi
Martin, Kathleen
Ho, Bryan
Bai, Hualong
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  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  surname: Li
  fullname: Li, Zhuo
  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
– sequence: 4
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  surname: Bai
  fullname: Bai, Hualong
  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  givenname: Luis
  surname: Gonzalez
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  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  surname: Ohashi
  fullname: Ohashi, Yuichi
  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  givenname: Masaki
  surname: Kano
  fullname: Kano, Masaki
  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  givenname: Bryan
  surname: Ho
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  organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT
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  email: alan.dardik@mountsinai.org
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Keywords Vascular remodeling
Arteriovenous fistula
Vascular identity
Venous graft
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Snippet Vascular remodeling is a dynamic process characterized by changes in vascular identity that impact vessel structure and function. Molecular markers define...
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SubjectTerms Arteriovenous fistula
Vascular identity
Vascular remodeling
Venous graft
Title Changes in vascular identity during vascular remodeling
URI https://dx.doi.org/10.1016/j.jvssci.2025.100282
https://www.ncbi.nlm.nih.gov/pubmed/40213096
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