Effects of Homocysteine on Proliferation, Necrosis, and Apoptosis of Vascular Smooth Muscle Cells in Culture and Influence of Folic Acid

Buemi, Michele; Marino, Domenico; Pasquale, Giuseppe Di; Floccari, Fulvio; Ruello, Antonella; Aloisi, Carmela; Corica, Francesco; Senatore, Massimino; Romeo, Adolfo; Frisina, N

doi:10.1016/s0049-3848(01)00363-2

Cited by 65 publications

(37 citation statements)

References 18 publications

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“…[14][15][16][17][18][19] Recent studies have now demonstrated that homocysteine causes endothelial cell dysfunction and induces apoptotic cell death in cell types relevant to atherothrombotic disease, including endothelial cells 22,23 and smooth muscle cells. 24 Furthermore, a direct causal relationship between induction of HHcy and accelerated atherosclerosis has been reported in apolipoprotein E (apoE)-deficient mice with diet-and/or genetic-induced HHcy. [25][26][27][28] Given that oral administration of folic acid or a combination of B vitamins can decrease HHcy and attenuate atherogenesis in these animal models, 26,28 there is growing interest for treatment of HHcy as a strategy for prevention of atherothrombotic disease.…”

Section: Introductionmentioning

confidence: 99%

Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease

2004

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Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease, including ischemic heart disease, stroke, and peripheral vascular disease. Mutations in the enzymes responsible for homocysteine metabolism, particularly cystathionine b-synthase (CBS) or 5,10-methylenetetrahydrofolate reductase (MTHFR), result in severe forms of HHcy. Additionally, nutritional deficiencies in B vitamin cofactors required for homocysteine metabolism, including folic acid, vitamin B6 (pyridoxal phosphate), and/or B12 (methylcobalamin), can induce HHcy. Studies using animal models of genetic-and diet-induced HHcy have recently demonstrated a causal relationship between HHcy, endothelial dysfunction, and accelerated atherosclerosis. Dietary enrichment in B vitamins attenuates these adverse effects of HHcy. Although oxidative stress and activation of proinflammatory factors have been proposed to explain the atherogenic effects of HHcy, recent in vitro and in vivo studies demonstrate that HHcy induces endoplasmic reticulum (ER) stress, leading to activation of the unfolded protein response (UPR). This review summarizes the current role of HHcy in endothelial dysfunction and explores the cellular mechanisms, including ER stress, that contribute to atherothrombosis.

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Section: Introductionmentioning

confidence: 99%

Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease

2004

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“…Importantly, a study by Buemi et al showed that HCY elevated both apoptosis and proliferation of VSMCs in vitro. 16 Clinically, atherosclerosis appeared to be associated with HCY levels of approximately 250 µM in hyperhomocysteinemic patients. [17][18][19] In addition, Yan et al 20 denoted that HCY (0.05-1 mM) elevated apoptosis of VSMCs in a dose-dependent manner.…”

Section: Commentarymentioning

confidence: 99%

Hyperhomocysteinemia and Alcoholism: A Double Hit?

Rezk¹,

Lucchesi²

2017

Toxicol Forensic Med Open J

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“…Homocysteine may cause endothelial injury [85], endothelial dysfunction [86,87], smooth muscle cell proliferation [88], and enhancement of vascular monocyte adhesion [89]. Homocysteine-induced oxidative stress plays a critical role in these processes [90,91].…”

Section: Insulin Resistancementioning

confidence: 99%

Multifactorial Determination of Hypertensive Nephroangiosclerosis

Tylicki

Rutkowski

Hörl

2002

Kidney Blood Press Res

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Essential hypertension causes renal injury. Hypertensive nephroangiosclerosis (HN) or hypertensive nephropathy are terms most commonly used to describe this renal pathology. Although specific histological lesions occurring in affected kidneys are well known, pathogenesis of hypertension-related renal scarring is not completely understood. Evidence exists to support the theory that other factors such as aging, black race or smoking, beside blood pressure, contribute to the development and progression of HN. Metabolic disturbances, cocaine and nonsteroidal anti-inflammatory drug abuse, ochratoxin A exposure, dietary salt intake, heavy metal toxicity, hantavirus infection and perinatal programming are also considered risk factors. Renal susceptibility genes may determine whether hypertension-induced progressive renal damage occurs and how severe it is. Determination of all risk factors may identify patients at high risk of renal failure and help tailor an appropriate management. In the present paper, the knowledge available on this clinically important objective is discussed.

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Effects of Homocysteine on Proliferation, Necrosis, and Apoptosis of Vascular Smooth Muscle Cells in Culture and Influence of Folic Acid

Cited by 65 publications

References 18 publications

Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease

Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease

Hyperhomocysteinemia and Alcoholism: A Double Hit?

Multifactorial Determination of Hypertensive Nephroangiosclerosis

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