التفاصيل البيبلوغرافية
| العنوان: |
Toxic effects of hyperhomocysteinemia in chronic renal failure and in uremia: cardiovascular and metabolic consequences |
| المؤلفون: |
Cinzia Lombardi, Rosanna Capasso, Eleonora Violetti, Filomena Acanfora, Natale G. De Santo, Diego Ingrosso, Alessandra F. Perna, Ersilia Satta, Maria Maddalena Romano |
| المساهمون: |
Perna, Alessandra, Capasso, R., Acanfora, F., Satta, E., Lombardi, C., Ingrosso, Diego, Violetti, E., Romano, M., DE SANTO, N. G. |
| المصدر: |
Seminars in nephrology. 26(1) |
| سنة النشر: |
2006 |
| مصطلحات موضوعية: |
Hyperhomocysteinemia, medicine.medical_specialty, Homocysteine, Hypomethylation, Biology, chemistry.chemical_compound, Metabolic Diseases, Internal medicine, Gene expression, Chronic renal failure, medicine, Humans, Receptor, Uremia, Folate receptor, Albumin, nutritional and metabolic diseases, food and beverages, medicine.disease, Blood proteins, Endocrinology, Uremic toxin, chemistry, Nephrology, Cardiovascular Diseases, Protein repair, Kidney Failure, Chronic |
| الوصف: |
Hyperhomocysteinemia, highly prevalent in well-nourished patients with chronic renal failure and in uremia, causes toxic effects that can be envisioned in terms of cardiovascular risk increase. However, its effects on cellular metabolism and on gene expression, not to mention receptor regulation, only recently are being evaluated. For example, it has been shown that hypomethylation induced by hyperhomocysteinemia can alter erythrocyte membrane protein repair and gene expression. In addition, increased plasma protein L-isoaspartyl content, related to hyperhomocysteinemia and uremic toxicity, determines specific effects on protein function, with a reduced binding of homocysteine to albumin. We propose that uremia is a state in which proteins present a widespread derangement of structure-function relationships. Hyperhomocysteinemia, highly prevalent in well-nourished patients with chronic renal failure and in uremia, causes toxic effects that can be envisioned in terms of cardiovascular risk increase. However, its effects on cellular metabolism and on gene expression, not to mention receptor regulation, only recently are being evaluated. For example, it has been shown that hypomethylation induced by hyperhomocysteinemia can alter erythrocyte membrane protein repair and gene expression. In addition, increased plasma protein L-isoaspartyl content, related to hyperhomocysteinemia and uremic toxicity, determines specific effects on protein function, with a reduced binding of homocysteine to albumin. We propose that uremia is a state in which proteins present a widespread derangement of structure-function relationships. © 2006 Elsevier Inc. All rights reserved. |
| تدمد: |
0270-9295 |
| الوصول الحر: |
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f77dbcde8a71834116dfe458c67c1f14Test
https://pubmed.ncbi.nlm.nih.gov/16412820Test |
| حقوق: |
CLOSED |
| رقم الانضمام: |
edsair.doi.dedup.....f77dbcde8a71834116dfe458c67c1f14 |
| قاعدة البيانات: |
OpenAIRE |
