细胞焦亡是新的程序性细胞死亡方式。lncRNAs参与该过程,机制不清楚。最近研究揭示 lncRNA通过编码肽发挥病理生理学作用。我们发现新lnc-rpS4编码肽rpS4xl参与肺动脉高压细胞焦亡，提示lnc-rpS4l通过编码肽rpS4xl的靶蛋白及靶蛋白互作网络调控平滑肌细胞焦亡。拟通过阐明lnc-rpS4l编码肽rpS4xl组织细胞分布特点及在细胞焦亡中的作用；rpS4xl靶蛋白核糖体蛋白S6（rpS6）的蛋白质互作网络；rpS4xl和rpS6互作的结构域和氨基酸位点，rpS4xl调控rpS6磷酸化和磷酸化位点，及这些结构域、氨基酸位点、磷酸化位点在细胞焦亡中的作用等证明该假设。本研究将首次探讨新lnc-rpS4l编码肽rpS4xl在肺动脉高压中的作用；阐明rpS4xl调控细胞焦亡的关键信号分子和机制，为肺动脉高压诊断和治疗提供潜在的靶点，并拓展lncRNAs在疾病中作用研究的新前沿。

Pyroptosis is an essential part of programmed cell death. Long chain non-coding RNAs (lncRNAs) is involved in the process. However, the role and mechanism of lncRNAs in regulation of pyroptosis are unclear. Recent evidence has demonstrated that functional peptides are encoded by short open reading frames (sORFs) in some lncRNAs, which play important roles in cell pathophysiological process. We found that the new lnc-rpS4l was involved in the pyroptosis of pulmonary arterial smooth muscle cells of pulmonary hypertension, and lnc-rpS4l encoded a small peptide rpS4xl, which regulates the cell pyroptosis. We hypothesis that lnc-rpS4l encoding peptide rpS4x1 regulate targeting protein rpS6 and the rpS6 network of target protein to promote pulmonary artery pyroptosis. The aim of this study was 1) to elucidate the origin and sequence, as well as tissue and cell distribution of lnc-rpS4l encoding peptide rpS4xl,2) to identify the role of lnc-rpS4l encoding peptide rpS4xl in cell pyroptosis,3) to reveal the target protein rpS6 and protein network regulated by lnc-rpS4l coding peptide rpS4xl,the domain and amino acid sites of the interaction between lnc-rpS4l encoding peptide rpS4xl and target protein. This study will explore the role of new lnc-rpS4l in pulmonary hypertension, and clarify the key signal molecules and action mechanisms of lnc-rpS4l encoding peptide rpS4xl, which provides a new solution and model for the study of the role of lncRNAs in disease.