非編碼核糖核酸參與心臟鈣穩(wěn)態(tài)調控機制的研究現狀
發(fā)布時間:2018-05-04 16:01
本文選題:鈣穩(wěn)態(tài) + 非編碼核糖核酸 ; 參考:《中國臨床藥理學雜志》2017年11期
【摘要】:心血管疾病發(fā)生率和致死率逐年增加,而目前的治療手段仍不足以解決這一現狀。Ca~(2+)是重要的第二信使,其穩(wěn)態(tài)失衡會導致細胞功能障礙和代謝紊亂,從而引起心臟功能異常,如心肌肥厚、心房纖顫、心肌缺血與心力衰竭等心血管疾病。蘭尼堿受體2(RyR2)、L型鈣通道(LTCC)、鈉鈣交換體(NCX)以及腺苷三磷酸(ATP)依賴性鈣泵(SERCA2a)等均能參與鈣穩(wěn)態(tài)的維持,然而更確切的調控機制仍未完全闡明,導致其在心血管疾病治療與預防應用中存在局限。非編碼核糖核酸(ncRNA)是一類不編碼蛋白的核糖核酸(RNA),可參與多種生物學功能。闡明非編碼RNA在鈣穩(wěn)態(tài)過程中的調控機制,有助于預測心房顫動等心臟疾病易感性、延緩病情進展及評估預后。本文對非編碼RNA參與心臟疾病鈣穩(wěn)態(tài)調控機制研究進展進行綜述。
[Abstract]:The incidence and mortality of cardiovascular diseases increase year by year, and the current treatment methods are not enough to solve this situation. Caan2) is an important second messenger. Its homeostasis can lead to cell dysfunction and metabolic disorder, which can lead to abnormal cardiac function. Such as myocardial hypertrophy, atrial fibrillation, myocardial ischemia and heart failure and other cardiovascular diseases. The L-type calcium channel of Lanni receptor 2N RyR2CX, sodium calcium exchanger NCX, and adenosine triphosphate ATP dependent calcium pump SERCA2a) can participate in the maintenance of calcium homeostasis. However, the more precise regulation mechanism has not been fully elucidated. These results in the limitation of its application in the treatment and prevention of cardiovascular diseases. Noncoding ribonucleic acid (ncRNAs) is a class of noncoding protein ribonucleic acid RNA (RNAs), which can participate in many biological functions. To elucidate the regulatory mechanism of noncoding RNA during calcium homeostasis is helpful to predict the susceptibility of atrial fibrillation and other heart diseases, delay the progression of the disease and evaluate the prognosis. This review reviews the progress of non-coding RNA in the regulation of calcium homeostasis in heart disease.
【作者單位】: 哈爾濱醫(yī)科大學藥理教研室;
【基金】:國家自然科學基金資助項目(81673426)
【分類號】:R54
【相似文獻】
相關期刊論文 前1條
1 孫小鵡;心肌細胞鈣穩(wěn)態(tài)研究新進展[J];實用醫(yī)技雜志;2005年09期
,本文編號:1843640
本文鏈接:http://sikaile.net/yixuelunwen/xxg/1843640.html
最近更新
教材專著