Androgen receptor (AR) in cardiovascular diseases.
Androgen receptor (AR) in cardiovascular diseases.
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DOI：
10.1530/joe-15-0518
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发表时间：
2016-04
期刊：
影响因子：
--
通讯作者：
Chang C
中科院分区：
文献类型：
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作者：
Huang CK;Lee SO;Chang E;Pang H;Chang C
心血管疾病（CVD）仍然是全球最主要的死亡原因。一些危险因素与心血管疾病有关，包括吸烟、糖尿病、高脂血症和性别等。性激素，特别是雄激素及其受体雄激素受体（AR），与许多疾病有明显的性别差异。在这里，我们总结了雄激素/AR对心血管疾病的影响，包括高血压，中风，动脉粥样硬化，腹主动脉瘤（AAA），心肌肥大，心力衰竭，以及代谢综合征/糖尿病及其对心血管疾病的影响。雄激素/AR信号转导可加重高血压，抗雄激素可抑制高血压。雄激素/AR信号在脑卒中中起着双重作用，这取决于不同类型的因素，但通常男性的脑卒中发病率高于女性。雄激素和AR差异调节动脉粥样硬化。雄激素缺乏导致脂质积聚升高，从而增强动脉粥样硬化，但在选择性细胞中靶向AR而不改变血清雄激素水平将抑制动脉粥样硬化进展。雄激素/AR信号传导在AAA的发生和进展中至关重要，靶向雄激素/AR可以极大地限制AAA的进展。与年龄匹配的女性相比，男性心脏肥大增加，这可能是由于雄激素。最后，雄激素/AR在促进肥胖和胰岛素/瘦素抵抗以增加代谢综合征中起重要作用。
Cardiovascular diseases (CVDs) are still the highest leading cause of death worldwide. Several risk factors have been linked to CVDs, including smoking, diabetes, hyperlipidemia, and gender among others. Sex hormones, especially the androgen and its receptor, androgen receptor (AR), have been linked to many diseases with a clear gender difference. Here, we summarize androgen/AR effects on CVDs, including hypertension, stroke, atherosclerosis, abdominal aortic aneurysm (AAA), myocardial hypertrophy, and heart failure, as well as metabolic syndrome/diabetes and their impacts on CVDs. Androgen/AR signaling exacerbates hypertension and anti-androgens may suppress hypertension. Androgen/AR signaling plays dual roles in strokes, depending on different kinds of factors, but generally males have a higher incidence of strokes than females. Androgen and AR differentially modulate atherosclerosis. Androgen deficiency causes elevated lipid accumulation to enhance atherosclerosis, but targeting AR in selective cells without altering serum androgen levels would suppress atherosclerosis progression. Androgen/AR signaling is crucial in AAA development and progression, and targeting androgen/AR profoundly restricts AAA progression. Men have increased cardiac hypertrophy as compared to age-matched women that may be due to androgens. Finally, androgen/AR plays important roles in contributing to obesity and insulin/leptin resistance to increase the metabolic syndrome.