The slowing down of renal deterioration but acceleration of cardiac hypertrophy: is the estrogen receptor-α a hero or villain?
| Autor: | Wen-Ling Lee, Ben-Shian Huang, Peng-Hui Peter Wang |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Kidney Contraction (grammar) Physiology medicine.drug_class business.industry Adenine Ischemia Estrogen receptor Glomerulosclerosis Renal function medicine.disease Endocrinology medicine.anatomical_structure Cardiovascular Diseases Estrogen Internal medicine medicine Animals Female Renal Insufficiency Chronic Endothelial dysfunction business |
| Zdroj: | American Journal of Physiology-Renal Physiology. 307:F1352-F1354 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.00529.2014 |
| Popis: | Role of estrogen receptor α (ERα) in the kidney and heart was still uncertain, although Estrogen-ER action is usually thought to function as reno- and possibly cardio-protection, which includes prevention of glomerulosclerosis and podocyte apoptosis in kidney, and atheroprotection by lowering plague formation and against endothelial dysfunction after injury, ischemia and re-perfusion. The adenine-fed rat model of Diwan showed that an adenine diet significantly decreased ERα expression in male rat kidney, but significantly increased ERα expression in the heart of both genders. Their results regarding renal function showed male adenine-fed rats had significantly more kidney function decline than female adenine-fed rats, suggesting the favorable role of ERα in the kidney. However, the results of an increased expression of ERα in the heart should be read with caution. Since an increased expression of ERα and the subsequently activating the extracellular signal-regulated kinase (ERK1/2) pathway may be attributed partly to cardiac hypertrophy. Cardiac hypertrophy, a compensation for the contraction ability of the heart, might transiently maintain the "normal" heart function; therefore, is a hero for the heart. However, cardiac hypertrophy may increase the burden of oxygen consumption and further exacerbate the severity of existence of ischemic heart disease or even worsen the "normal heart". Therefore, the net long-term effect of ERα might not be good for the heart itself. |
| Databáze: | OpenAIRE |
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