Epigenetics, the missing link in hypertension

Raftopoulos, Leonidas; Katsi, Vasiliki; Makris, Thomas; Tousoulis, Dimitrios; Stefanadis, Christodoulos; Kallikazaros, Ioannis

doi:10.1016/j.lfs.2014.08.003

Cited by 44 publications

(45 citation statements)

References 41 publications

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“…Although epigenetics play a crucial role on kidney development and hypertension [29,30], to the best of our knowledge, our study is the first to show DEX-induced changes on the developing epigenome in the kidney. Glucocorticoids can modify the fetal epigenome through direct action on the glucocorticoid response element (GRE) or indirect regulation through the expression of epigenetic regulator genes [12].…”

Section: Discussionmentioning

confidence: 63%

Prenatal dexamethasone-induced programmed hypertension and renal programming

Sheen

Tiao

et al. 2015

Life Sciences

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Section: Discussionmentioning

confidence: 63%

Prenatal dexamethasone-induced programmed hypertension and renal programming

Sheen

Tiao

et al. 2015

Life Sciences

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“…Hypertension is a multifactorial, worldwide health problem that involves genetic and epigenetic factors, unhealthy diets, lifestyle factors and excess weight [1,2,3]. Initially, the vascular remodeling caused by increasing blood pressure is beneficial as it allows vessels to adapt to transient hemodynamic changes [4].…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase 2 as a Potential Mediator of Vascular Smooth Muscle Cell Migration and Chronic Vascular Remodeling in Hypertension

Belo¹,

Guimaraes²,

Castro³

2015

J Vasc Res

111

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For vascular remodeling in hypertension, it is essential that vascular smooth muscle cells (VSMCs) reshape in order to proliferate and migrate. The extracellular matrix (ECM) needs to be degraded to favor VSMC migration. Many proteases, including matrix metalloproteinases (MMPs), contribute to ECM proteolysis and VSMC migration. Bioactive peptides, hemodynamic forces and reactive oxygen-nitrogen species regulate MMP-2 expression and activity. Increased MMP-2 activity contributes to hypertension-induced maladaptive arterial changes and sustained hypertension. New ECM is synthesized to supply VSMCs with bioactive mediators, which stimulate hypertrophy. MMP-2 stimulates the interaction of VSMCs with newly formed ECM, which triggers intracellular signaling via integrins to induce a phenotypic switch and persistent migration. VSMCs switch from a contractile to a synthetic phenotype in order to migrate and contribute to vascular remodeling in hypertension. MMPs also disrupt growth factors bound to ECM, thus contributing to their capacity to regulate VSMC migration. This review sheds light on the proteolytic effects of MMP-2 on ECM and non-ECM substrates in the vasculature and how these effects contribute to VSMC migration in hypertension. The inhibition of MMP activity as a therapeutic target may make it possible to reduce arterial maladaptation caused by hypertension and prevent the resulting fatal cardiovascular events.

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“…-АГ [1,13]. Навколишнє середовище впливає на серцево-судинну систему, може викликати такі патологічні стани, як атеросклероз або інфаркт міокарда [14].…”

Section: основні епігенетичні механізми розвитку артеріальної гіпертеunclassified