上周（2026年2月2日至2月6日）全球生物医药重大突破

上周，顶级科学期刊发布多项生物医药领域里程碑式成果。

2月4日，美国德克萨斯大学西南医学中心陈志坚团队发表于《自然》的研究表明，磷脂酰肌醇3,5-二磷酸（PtdIns(3,5)P2）是STING蛋白的内源性配体，明确了先天免疫中STING通路的内源性激活分子基础。该发现填补了STING内源性配体的研究空白，为精准调控先天免疫通路提供了核心靶点，为炎症性疾病、自身免疫病及肿瘤的靶向药物研发奠定关键理论基础。陈志坚教授生于福建安溪，美国国家科学院和医学院院士，核心贡献是发现cGAS-STING通路，阐明DNA驱动先天免疫与炎症的机制 。2024年获得诺贝尔奖风向标之一的拉斯克基础医学研究奖，表彰发现cGAS酶及DNA免疫激活机制；同年，获得德国医学重要奖项保罗·埃尔利希和路德维希·达姆施泰特奖。2026年获得日本国际奖（Japan Prize，也被称为诺贝尔奖风向标之一），表彰先天免疫核酸感知机制研究。

2月4日，北京大学和郑州大学团队的《自然》文章，提出帕金森病（PD）是躯体-认知-行动网络（SCAN）障碍。团队分析863例患者影像数据，发现PD核心是SCAN与皮质下运动相关脑区异常过度连接，此为PD特异性标志，区别于特发性震颤等其他运动障碍 。研究证实，所有有效疗法均能降低该异常连接，为精准神经调控治疗提供全新框架。

2月4日，美国宾夕法尼亚大学和耶鲁大学团队的《自然》文章揭示，肺癌细胞劫持神经通路向大脑发送虚假信号。癌细胞可劫持迷走感觉-交感神经轴，形成“肿瘤→脑→肿瘤”的免疫抑制环路。癌细胞激活表达Npy2r的迷走感觉神经元，经脑干孤束核等传递信号，驱动交感神经释放去甲肾上腺素，作用于肺泡巨噬细胞β2肾上腺素能受体，抑制抗肿瘤T细胞反应，促进肿瘤生长。小鼠实验显示，破坏该通路可显著抑制肿瘤生长，且在人类肺腺癌样本中验证了该环路存在。这为癌症治疗提供神经免疫靶点新方向。

2月4日，CORALreef Lipids发表于《新英格兰医学杂志》研究，表明口服PCSK9抑制剂enlicitide decanoate具有良好降脂效果，治疗第24周时，低密度脂蛋白胆固醇（ 俗称“坏胆固醇”）平均水平较基线降低57.1%，这一趋势维持到治疗第52周，且安全性可控。从而，PCSK9抑制剂降脂进入“口服时代”。低密度脂蛋白胆固醇是动脉粥样硬化心血管疾病发生、发展的主要危险因素。

2月5日，复旦大学团队的《细胞》文章，揭示感觉神经通过肿瘤相关成纤维细胞构建致密细胞外基质，导致三阴性乳腺癌免疫排斥与免疫治疗耐药。值得关注的是，研究中采用的神经信号抑制剂——瑞美吉泮（CGRP受体拮抗剂），是一款广泛用于偏头痛治疗的药物，具备成熟的临床安全性数据。老药新用，有望缩短临床转化周期，让科研成果快速落地，造福患者。

这些集中发布的文章从基础机制到临床转化全面突破，为相关疾病的诊断与治疗开辟了新路径。

Major Breakthroughs in Global Biomedicine Last Week (February 2–6, 2026)

A series of landmark findings in biomedicine were released by top scientific journals last week, covering fundamental mechanistic research to clinical translation and pioneering new paths for the diagnosis and treatment of various diseases.

On February 4, the team of Zhijian James Chen from UT Southwestern Medical Center published a study in Nature, identifying phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2) as the endogenous ligand of the STING protein. This discovery clarifies the molecular basis for the endogenous activation of the STING pathway in innate immunity, fills the research gap in the endogenous ligands of STING, provides a core target for the precise regulation of innate immune pathways, and lays a critical theoretical foundation for the development of targeted drugs for inflammatory diseases, autoimmune diseases and tumors. Born in Anxi, Fujian, China, Prof. Chen is a member of the US National Academy of Sciences and the US National Academy of Medicine, whose seminal contribution is the discovery of the cGAS-STING pathway and the elucidation of the mechanism of DNA-driven innate immunity and inflammation. He was awarded the 2024 Lasker Basic Medical Research Award (a renowned precursor to the Nobel Prize) for the discovery of the cGAS enzyme and the DNA-mediated immune activation mechanism, and the Paul Ehrlich and Ludwig Darmstaedter Prize (a major German medical award) in the same year. In 2026, he won the Japan Prize (another Nobel Prize precursor) in recognition of his research on the nucleic acid sensing mechanism of innate immunity.

Also on February 4, a joint team from Peking University and Zhengzhou University published a paper in Nature, proposing that Parkinson's disease (PD) is a disorder of the Somatic-Cognitive-Action Network (SCAN). By analyzing imaging data from 863 PD patients, the team found that the core pathological feature of PD is abnormally excessive connectivity between the SCAN and subcortical motor-related brain regions—a specific marker for PD that distinguishes it from other movement disorders such as essential tremor. The study confirmed that all effective PD therapies can reduce this abnormal connectivity, providing a novel framework for precise neuromodulation treatment of the disease.

On February 4, teams from the University of Pennsylvania and Yale University published a research in Nature, revealing that lung cancer cells hijack neural pathways to send false signals to the brain. Cancer cells can usurp the vagal sensory-sympathetic neural axis to form an immunosuppressive loop of "tumor→brain →tumor". Specifically, cancer cells activate Npy2r-expressing vagal sensory neurons, which transmit signals through the nucleus of the solitary tract in the brainstem and other regions, driving sympathetic nerves to release norepinephrine. Norepinephrine then acts on the β2-adrenergic receptor of alveolar macrophages, inhibiting the anti-tumor T cell response and promoting tumor growth. Mouse experiments showed that disrupting this pathway significantly suppresses tumor growth, and the existence of this loop was verified in human lung adenocarcinoma samples, opening up a new direction for identifying neuro-immune targets in cancer therapy.

Likewise on February 4, CORALreef Lipids published a study in the New England Journal of Medicine, demonstrating that enlicitide decanoate, an oral PCSK9 inhibitor, exerts a favorable lipid-lowering effect. At week 24 of treatment, the average level of low-density lipoprotein cholesterol (LDL-C, commonly known as "bad cholesterol") was reduced by 57.1% compared with the baseline, and this trend was sustained up to week 52, with a manageable safety profile. This breakthrough ushers in the oral era for PCSK9 inhibitor-based lipid-lowering therapy. LDL-C is a major risk factor for the development and progression of atherosclerotic cardiovascular diseases.

On February 5, the team from Fudan University published a paper in Cell, uncovering that sensory nerves construct a dense extracellular matrix through cancer-associated fibroblasts, leading to immune exclusion and immunotherapy resistance in triple-negative breast cancer (TNBC). Notably, rimegepant—a CGRP receptor antagonist used in the study as a neural signal inhibitor—is a widely prescribed drug for migraine with well-established clinical safety data. This repurposing of an existing drug is expected to shorten the clinical translation cycle and accelerate the clinical application of scientific research findings to benefit patients.

The above findings represent comprehensive breakthroughs in biomedicine from basic mechanism exploration to clinical translation, opening up new avenues for the diagnosis, treatment and drug development of inflammatory diseases, neurological disorders, malignant tumors and cardiovascular diseases.