Mechanisms of the Multitasking Endothelial Protein NRG-1 as a Compensatory Factor during Chronic Heart Failure
De K. G. W., Feyen E., Dugaucquier L., Shakeri H., Shhendry'gina A. A., Belenkov Yu. N., Brink M., Vermeulen Z., Segers V. F. M.
Circulation: Heart Failure
Vol.12, Issue10, Num.e006288
Опубликовано: 2019
Тип ресурса: Статья
DOI:10.1161/CIRCHEARTFAILURE.119.006288
Аннотация:
Heart failure is a complex syndrome whose phenotypic presentation and disease progression depends on a complex network of adaptive and maladaptive responses. One of these responses is the endothelial release of NRG (neuregulin)-1 - a paracrine growth factor activating ErbB2 (erythroblastic leukemia viral oncogene homolog B2), ErbB3, and ErbB4 receptor tyrosine kinases on various targets cells. NRG-1 features a multitasking profile tuning regenerative, inflammatory, fibrotic, and metabolic processes. Here, we review the activities of NRG-1 on different cell types and organs and their implication for heart failure progression and its comorbidities. Although, in general, effects of NRG-1 in heart failure are compensatory and beneficial, translation into therapies remains unaccomplished both because of the complexity of the underlying pathways and because of the challenges in the development of therapeutics (proteins, peptides, small molecules, and RNA-based therapies) for tyrosine kinase
Ключевые слова:
Disease progression; endothelium; heart failure; neuregulin-1; receptor protein-tyrosine kinases; receptor, ErbB4
epidermal growth factor receptor 2; epidermal growth factor receptor 3; epidermal growth factor receptor 4; neu differentiation factor; tyrosine kinase receptor; cardiovascular agent; epidermal growth factor receptor; ligand; neu differentiation factor; Article; atherosclerosis; cardiac muscle cell; cell survival; comorbidity; diabetes mellitus; disease exacerbation; drug efficacy; fibroblast; fibrosis; heart failure; heart right ventricle failure; human; inflammation; kidney failure; macrophage; nonhuman; pulmonary hypertension; signal transduction; smooth muscle cell; tissue regeneration; vascular endothelial cell; animal; chronic disease; drug effect; endothelium cell; heart failure; metabolism; molecularly targeted therapy; pathophysiology; Animals; Cardiovascular Agents; Chronic Disease; Endothelial Cells; ErbB Receptors; Heart Failure; Humans; Ligands; Molecular Targeted Therapy; Neuregulin-1; Signal Transduction
Язык текста: Английский
ISSN: 1941-3297
De K. G. W. Keulenaer G.W.
Feyen E.
Dugaucquier L.
Shakeri H.
Shhendry'gina A. A. Anastasiya Aleksandrovna 1984-
Belenkov Yu. N. Yurij Nikitich 1948-
Brink M.
Vermeulen Z.
Segers V. F. M.
Де К. Г. W. Кеуленаер Г.W.
Феьен Е.
Дугауcqуиер Л.
Шакери Х.
Щендрыгина А. А. Анастасия Александровна 1984-
Беленков Ю. Н. Юрий Никитич 1948-
Бринк М.
Вермеулен З.
Сегерс В. Ф. М.
Mechanisms of the Multitasking Endothelial Protein NRG-1 as a Compensatory Factor during Chronic Heart Failure
Текст визуальный непосредственный
Circulation: Heart Failure
Lippincott Williams & Wilkins Ltd.
Vol.12, Issue10 Num.e006288
2019
Статья
Disease progression endothelium heart failure neuregulin-1 receptor protein-tyrosine kinases receptor, ErbB4
epidermal growth factor receptor 2 epidermal growth factor receptor 3 epidermal growth factor receptor 4 neu differentiation factor tyrosine kinase receptor cardiovascular agent epidermal growth factor receptor ligand neu differentiation factor Article atherosclerosis cardiac muscle cell cell survival comorbidity diabetes mellitus disease exacerbation drug efficacy fibroblast fibrosis heart failure heart right ventricle failure human inflammation kidney failure macrophage nonhuman pulmonary hypertension signal transduction smooth muscle cell tissue regeneration vascular endothelial cell animal chronic disease drug effect endothelium cell heart failure metabolism molecularly targeted therapy pathophysiology Animals Cardiovascular Agents Chronic Disease Endothelial Cells ErbB Receptors Heart Failure Humans Ligands Molecular Targeted Therapy Neuregulin-1 Signal Transduction
Heart failure is a complex syndrome whose phenotypic presentation and disease progression depends on a complex network of adaptive and maladaptive responses. One of these responses is the endothelial release of NRG (neuregulin)-1 - a paracrine growth factor activating ErbB2 (erythroblastic leukemia viral oncogene homolog B2), ErbB3, and ErbB4 receptor tyrosine kinases on various targets cells. NRG-1 features a multitasking profile tuning regenerative, inflammatory, fibrotic, and metabolic processes. Here, we review the activities of NRG-1 on different cell types and organs and their implication for heart failure progression and its comorbidities. Although, in general, effects of NRG-1 in heart failure are compensatory and beneficial, translation into therapies remains unaccomplished both because of the complexity of the underlying pathways and because of the challenges in the development of therapeutics (proteins, peptides, small molecules, and RNA-based therapies) for tyrosine kinase