肾衰竭导致大鼠心脏端粒缩短。
Renal failure induces telomere shortening in the rat heart.
机构信息
Department of Cardiology, University Medical Center Groningen, Groningen, the Netherlands.
出版信息
Neth Heart J. 2009 May;17(5):190-4. doi: 10.1007/BF03086245.
BACKGROUND
Renal failure aggravates pathological cardiac remodelling induced by myocardial infarction (MI). Cardiac remodelling is associated with telomere shortening, a marker for biological ageing. We investigated whether mild and severe renal failure shorten cardiac telomeres and excessively shorten telomeres after MI.
METHODS
Rats were subjected to sham, unilateral (UNX) or 5/6th nephrectomy (5/6NX) to induce none, mild or severe renal failure. MI was induced by left coronary artery ligation. Renal function parameters and blood pressure were measured. DNA was isolated from non-infarcted cardiac tissue. Telomere length was assessed by quantitative polymerase chain reaction (PCR).
RESULTS
Proteinuria was unchanged in UNX and MI compared with control, but strongly increased in 5/6NX, UNX+MI and 5/6NX+MI. Serum creatinine levels were increased fourfold in 5/6NX and tenfold in 5/6NX+MI. 5/6NX and groups with both renal failure and MI showed an approximate 20% reduction of telomere length, similar to the MI group. No excess telomere shortening was observed in hearts from rats with renal ablation after MI.
CONCLUSION
Severe renal failure, but not mild renal failure, leads to shortening of cardiac telomeres to a similar extent as found after MI. Renal failure did not induce excessive telomere shortening after MI. (Neth Heart J 2009;17:190-4.).
背景
肾衰竭会加重心肌梗死（MI）引起的病理性心脏重构。心脏重构与端粒缩短有关，端粒缩短是生物衰老的标志。我们研究了轻度和重度肾衰竭是否会缩短心脏端粒，以及 MI 后是否会过度缩短端粒。
方法
大鼠接受假手术、单侧（UNX）或 5/6 肾切除术（5/6NX），以诱导无、轻度或重度肾衰竭。通过左冠状动脉结扎诱导 MI。测量肾功能参数和血压。从非梗塞性心脏组织中分离 DNA。通过定量聚合酶链反应（PCR）评估端粒长度。
结果
与对照组相比，UNX 和 MI 时蛋白尿没有变化，但在 5/6NX、UNX+MI 和 5/6NX+MI 中则明显增加。5/6NX 中血清肌酐水平增加了四倍，在 5/6NX+MI 中增加了十倍。5/6NX 和同时存在肾衰竭和 MI 的组的端粒长度减少了大约 20%，与 MI 组相似。在 MI 后进行肾消融的大鼠心脏中没有观察到端粒过度缩短。
结论
严重肾衰竭而非轻度肾衰竭会导致心脏端粒缩短，与 MI 后发现的程度相似。肾衰竭不会在 MI 后引起端粒过度缩短。（Neth Heart J 2009;17:190-4.）。
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