Mechanisms and Clinical Implications of Endothelial Dysfunction in Arterial Hypertension
The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed a...
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Published in | Journal of cardiovascular development and disease Vol. 9; no. 5; p. 136 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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27.04.2022
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Abstract | The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities. |
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AbstractList | The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities. The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities.The endothelium is composed of a monolayer of endothelial cells, lining the interior surface of blood and lymphatic vessels. Endothelial cells display important homeostatic functions, since they are able to respond to humoral and hemodynamic stimuli. Thus, endothelial dysfunction has been proposed as a key and early pathogenic mechanism in many clinical conditions. Given the relevant repercussions on cardiovascular risk, the complex interplay between endothelial dysfunction and systemic arterial hypertension has been a matter of study in recent years. Numerous articles have been published on this issue, all of which contribute to providing an interesting insight into the molecular mechanisms of endothelial dysfunction in arterial hypertension and its role as a biomarker of inflammation, oxidative stress, and vascular disease. The prognostic and therapeutic implications of endothelial dysfunction have also been analyzed in this clinical setting, with interesting new findings and potential applications in clinical practice and future research. The aim of this review is to summarize the pathophysiology of the relationship between endothelial dysfunction and systemic arterial hypertension, with a focus on the personalized pharmacological and rehabilitation strategies targeting endothelial dysfunction while treating hypertension and cardiovascular comorbidities. |
Author | Ambrosino, Pasquale Perrotta, Fabio Motta, Andrea Maniscalco, Mauro D’Agnano, Vito Galloway, Brurya Bachetti, Tiziana D’Anna, Silvestro Ennio Bianco, Andrea Papa, Antimo |
AuthorAffiliation | 2 Istituti Clinici Scientifici Maugeri IRCCS, Scientific Direction, 27100 Pavia, Italy; tiziana.bachetti@icsmaugeri.it 1 Istituti Clinici Scientifici Maugeri IRCCS, Cardiac Rehabilitation Unit of Telese Terme Institute, 82037 Telese Terme, Italy; antimo.papa@icsmaugeri.it 3 Istituti Clinici Scientifici Maugeri IRCCS, Pulmonary Rehabilitation Unit of Telese Terme Institute, 82037 Telese Terme, Italy; silvestro.danna@icsmaugeri.it 5 Institute of Biomolecular Chemistry, National Research Council, 80078 Pozzuoli, Italy; andrea.motta@icb.cnr.it 4 Department of Translational Medical Sciences, University of Campania “Luigi Vanvitelli”, 80131 Naples, Italy; brurya29@gmail.com (B.G.); andrea.bianco@unicampania.it (A.B.); vito.dagnano94@gmail.com (V.D.); fabio.perrotta@unicampania.it (F.P.) 6 Department of Clinical Medicine and Surgery, “Federico II” University, 80131 Naples, Italy |
AuthorAffiliation_xml | – name: 4 Department of Translational Medical Sciences, University of Campania “Luigi Vanvitelli”, 80131 Naples, Italy; brurya29@gmail.com (B.G.); andrea.bianco@unicampania.it (A.B.); vito.dagnano94@gmail.com (V.D.); fabio.perrotta@unicampania.it (F.P.) – name: 6 Department of Clinical Medicine and Surgery, “Federico II” University, 80131 Naples, Italy – name: 2 Istituti Clinici Scientifici Maugeri IRCCS, Scientific Direction, 27100 Pavia, Italy; tiziana.bachetti@icsmaugeri.it – name: 3 Istituti Clinici Scientifici Maugeri IRCCS, Pulmonary Rehabilitation Unit of Telese Terme Institute, 82037 Telese Terme, Italy; silvestro.danna@icsmaugeri.it – name: 5 Institute of Biomolecular Chemistry, National Research Council, 80078 Pozzuoli, Italy; andrea.motta@icb.cnr.it – name: 1 Istituti Clinici Scientifici Maugeri IRCCS, Cardiac Rehabilitation Unit of Telese Terme Institute, 82037 Telese Terme, Italy; antimo.papa@icsmaugeri.it |
Author_xml | – sequence: 1 givenname: Pasquale orcidid: 0000-0002-9398-0428 surname: Ambrosino fullname: Ambrosino, Pasquale – sequence: 2 givenname: Tiziana orcidid: 0000-0003-1612-5329 surname: Bachetti fullname: Bachetti, Tiziana – sequence: 3 givenname: Silvestro Ennio surname: D’Anna fullname: D’Anna, Silvestro Ennio – sequence: 4 givenname: Brurya surname: Galloway fullname: Galloway, Brurya – sequence: 5 givenname: Andrea orcidid: 0000-0002-4692-5901 surname: Bianco fullname: Bianco, Andrea – sequence: 6 givenname: Vito surname: D’Agnano fullname: D’Agnano, Vito – sequence: 7 givenname: Antimo surname: Papa fullname: Papa, Antimo – sequence: 8 givenname: Andrea orcidid: 0000-0002-8643-658X surname: Motta fullname: Motta, Andrea – sequence: 9 givenname: Fabio orcidid: 0000-0002-7223-7037 surname: Perrotta fullname: Perrotta, Fabio – sequence: 10 givenname: Mauro orcidid: 0000-0001-6751-9921 surname: Maniscalco fullname: Maniscalco, Mauro |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35621847$$D View this record in MEDLINE/PubMed |
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Keywords | arterial hypertension cardiovascular disease heart failure rehabilitation arginine chronic disease exercise endothelial dysfunction occupational medicine outcome |
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