發(fā)布時(shí)間：2018-05-02 18:25

  本文選題：低氧 + 肺動(dòng)脈高壓��； 參考：《第四軍醫(yī)大學(xué)》2006年碩士論文

【摘要】：肺動(dòng)脈高壓(pulmonary arterial hypertension，PAH)是由多種原因引起的肺部血液循環(huán)動(dòng)力學(xué)的功能紊亂，以肺血管阻力進(jìn)行性增加為臨床特征的一組疾病，也是肺循環(huán)中最嚴(yán)重，具有最大潛在危險(xiǎn)性的慢性疾病，可導(dǎo)致肺源性心臟病，右心衰竭，引起過(guò)早死亡。已有的研究表明低氧是引起肺動(dòng)脈高壓的重要原因之一。低氧所致的PAH的發(fā)病過(guò)程包括：肺部血管收縮、肺動(dòng)脈平滑肌細(xì)胞(pulmonary arterial smooth muscle cells，PASMCs)肥大和增生及肺部血管的重建。 目前研究認(rèn)為，，PASMCs增殖和凋亡的失衡是導(dǎo)致PASMCs增殖累積和肺部血管壁重建的重要因素之一。因此，抑制PASMCs過(guò)度增殖，誘導(dǎo)其凋亡可以作為治療和控制PAH的有效方法。腫瘤抑制基因p53在誘導(dǎo)細(xì)胞凋亡中具有一定作用。它是一種多效性的轉(zhuǎn)錄因子，在特定條件下具有決定細(xì)胞命運(yùn)的重要作用：一方面是抑制細(xì)胞分裂，讓其停留在細(xì)胞周期的G_1期；另一方面是促使細(xì)胞凋亡。p53基因有野生型(wild-type 53，wtp53)和突變型(mutant-type 53，mtp53)兩種。wtp53為抑癌基因，對(duì)細(xì)胞分裂和增殖起負(fù)調(diào)節(jié)作用，還能啟動(dòng)細(xì)胞的程序性死亡過(guò)程，防止細(xì)胞惡性轉(zhuǎn)化。mtp53抑癌功能喪失，失去對(duì)細(xì)胞異常增殖的抑制作用，它通過(guò)正信號(hào)調(diào)節(jié)作用，促進(jìn)細(xì)胞進(jìn)入增生周期，促進(jìn)細(xì)胞
[Abstract]:Pulmonary arterial hypertensionPAH (PAHs) is a group of diseases characterized by progressive increase of pulmonary vascular resistance, which is caused by various causes and is the most serious of pulmonary circulation. Chronic diseases with the greatest potential risk can lead to pulmonary heart disease, right heart failure, and premature death. Studies have shown that hypoxia is one of the important causes of pulmonary hypertension. The pathogenesis of hypoxic PAH includes pulmonary vasoconstriction and pulmonary arterial smooth muscle. PASMCs) hypertrophy and proliferation and pulmonary vascular remodeling. It is suggested that the imbalance between proliferation and apoptosis of PASMCs is one of the important factors leading to the accumulation of PASMCs proliferation and the remodeling of pulmonary vascular wall. Therefore, inhibiting the excessive proliferation of PASMCs and inducing its apoptosis may be an effective method for the treatment and control of PAH. Tumor suppressor gene p53 plays an important role in inducing apoptosis. It is a multifunctional transcription factor, which plays an important role in determining the fate of cells under certain conditions: on the one hand, it inhibits cell division and keeps it in the GSP 1 phase of cell cycle; On the other hand, there are wild type wild-type 53 (wtp53) and mutant mutant-type 53 (mtp53). Wtp53 is a tumor suppressor gene, which plays a negative role in cell division and proliferation, and can initiate the programmed cell death process. It can prevent the cell malignant transformation. Mtp53 from losing the function of inhibiting the cell proliferation. It can promote the cell into the proliferative cycle and promote the cell through the positive signal regulation.
【學(xué)位授予單位】：第四軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 顧勇,劉秀琴,孫培吾,張希,童萃文;肺高壓大鼠血漿中ET、ANP和CGRP含量變化的相關(guān)研究[J];標(biāo)記免疫分析與臨床;2000年04期

2 彭利靜;李志超;李偉;李志斌;閆志強(qiáng);張齊;劉毅;羅穎;;慢性低氧性肺動(dòng)脈高壓大鼠體內(nèi)血管活性物質(zhì)表達(dá)的變化及意義[J];第四軍醫(yī)大學(xué)學(xué)報(bào);2006年05期

3 張振峰,張承惠;p53與人類肺癌研究進(jìn)展[J];國(guó)外醫(yī)學(xué)(內(nèi)科學(xué)分冊(cè));1999年06期

4 楊炯,鮮云艷,胡蘇萍,李明震;降鈣素基因相關(guān)肽對(duì)慢性缺氧性肺動(dòng)脈高壓的作用[J];湖北醫(yī)科大學(xué)學(xué)報(bào);1997年04期

5 宋海邦,瓦龍美;低氧條件下低氧誘導(dǎo)因子-1α及p53的表達(dá)[J];解剖學(xué)報(bào);2004年03期

6 陸慰萱;;肺動(dòng)脈高壓的新分類[J];中國(guó)實(shí)用內(nèi)科雜志;2006年01期

7 王望,王憲;降鈣素基因相關(guān)肽超家族與高血壓[J];心血管病學(xué)進(jìn)展;2000年05期

8 李曉艷,黃從新,孫有剛,王晉明,王晶,王騰;降鈣素基因相關(guān)肽對(duì)人血管平滑肌細(xì)胞增殖的抑制作用[J];中國(guó)病理生理雜志;2000年01期

9 鐘小寧,姚龍;肺血管重建在低氧性肺動(dòng)脈高壓中的作用及其機(jī)制[J];中國(guó)呼吸與危重監(jiān)護(hù)雜志;2003年04期

10 李榮,別畢華,彭則,張珍祥;野生型p53、bcl_2基因在低氧性肺動(dòng)脈高壓大鼠肺內(nèi)表達(dá)及其分布[J];中國(guó)應(yīng)用生理學(xué)雜志;2000年03期

本文編號(hào)：1834994