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 in | JVS-vascular science Vol. 6; p. 100282 |
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01.01.2025
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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.
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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 |
Author_xml | – sequence: 1 givenname: Yukihiko surname: Aoyagi fullname: Aoyagi, Yukihiko organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 2 givenname: Andrew W. orcidid: 0000-0003-3846-5877 surname: Schwartz fullname: Schwartz, Andrew W. organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 3 givenname: Zhuo surname: Li fullname: Li, Zhuo organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 4 givenname: Hualong surname: Bai fullname: Bai, Hualong organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 5 givenname: Luis surname: Gonzalez fullname: Gonzalez, Luis organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 6 givenname: Cayetana surname: Lazcano Etchebarne fullname: Lazcano Etchebarne, Cayetana organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 7 givenname: Yuichi surname: Ohashi fullname: Ohashi, Yuichi organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 8 givenname: Masaki surname: Kano fullname: Kano, Masaki organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 9 givenname: Bryan surname: Ho fullname: Ho, Bryan organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 10 givenname: Kathleen surname: Martin fullname: Martin, Kathleen organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT – sequence: 11 givenname: Alan surname: Dardik fullname: Dardik, Alan email: alan.dardik@mountsinai.org organization: Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40213096$$D View this record in MEDLINE/PubMed |
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Keywords | Vascular remodeling Arteriovenous fistula Vascular identity Venous graft |
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SubjectTerms | Arteriovenous fistula Vascular identity Vascular remodeling Venous graft |
Title | Changes in vascular identity during vascular remodeling |
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