细胞核中的自救刹车！陈玲玲团队最新Cell论文揭开核应激小体的动态组装及其对急性炎症的调控机制

Core Viewpoint - The research highlights the role of nuclear stress bodies (nSB) in regulating gene expression and suppressing acute inflammatory responses, providing new insights for the diagnosis and treatment of sepsis [3][12][16]. Group 1: Mechanism of nSB Formation - Under stress conditions such as heat shock and arsenic poisoning, human cells rapidly form a membrane-less structure known as nuclear stress bodies (nSB) [7]. - The nSB is composed of a core layer of Satellite III (SatIII) RNA, a regulatory layer with transcription factors like HSF1, and an outer layer of proteins such as SAFB that maintain structural stability [7][9]. Group 2: Gene Expression Regulation - The formation of nSB leads to a significant increase in the expression of the NFIL3 gene, which can rise up to 8 times [11]. - NFIL3 plays a crucial role in inhibiting the expression of inflammatory factors such as TNF-α and IL-1β, with its knockout resulting in a 300% increase in inflammation intensity [11]. Group 3: Clinical Implications for Sepsis - A study involving 150 sepsis patients revealed that the activation of SatIII and the assembly of nSB correlate positively with patient survival rates [13][14]. - Patients with high SatIII expression showed a 65% increase in 28-day survival rates, indicating the potential of nSB as a survival marker in sepsis [14][16].