Zhao Renjia, Lu Heyang, Yuan Huangbo, Chen Shuaizhou, Xu Kelin, Zhang Tiejun, Liu Zhenqiu, Jiang Yanfeng, Suo Chen, Chen Xingdong
State Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Songhu Road 2005, Shanghai, China.
Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Geroscience. 2025 Apr;47(2):1411-1423. doi: 10.1007/s11357-024-01411-w. Epub 2024 Oct 31.
Individual's aging rates vary across organs. However, there are few methods for assessing aging at organ levels and whether they contribute differently to mortalities remains unknown. We analyzed data from 45,821 adults in the UK Biobank, using plasma proteomics and machine learning to estimate biological ages for 12 major organs. The differences between biological age and chronological age, referred to as "age gaps," were calculated for each organ. Partial correlation analyses were used to assess the association between age gaps and modifiable factors. Adjusted multivariable Cox regression models were applied to examine the association of age gaps with all-cause mortality, cause-specific mortalities, and cancer-specific mortalities. We reveal a complex network of varied associations between multi-organ aging and modifiable factors. All age gaps increase the risk of all-cause mortality by 6-60%. The risk of death varied from 5.54 to 29.18 times depending on the number of aging organs. Cause-specific mortalities are associated with certain organs' aging. For mental diseases mortality, and nervous system mortality, only brain aging exhibited a significant increased risk of HR 2.38 (per SD, 95% CI: 2.06-2.74) and 1.99 (per SD, 95% CI: 1.84-2.16), respectively. Age gaps of stomach were also a specific indicator for gastric cancer. Eventually, we find that an organ's biological age selectively influences the aging of other organ systems. Our study demonstrates that accelerated aging in specific organs increases the risk of mortality from various causes. This provides a potential tool for early identification of at-risk populations, offering a relatively objective method for precision medicine.
个体的衰老速度因器官而异。然而,评估器官水平衰老的方法很少,而且它们对死亡率的贡献是否不同仍不清楚。我们分析了英国生物银行中45821名成年人的数据,使用血浆蛋白质组学和机器学习来估计12个主要器官的生物学年龄。计算每个器官的生物学年龄与实际年龄之间的差异,即“年龄差距”。采用偏相关分析评估年龄差距与可改变因素之间的关联。应用调整后的多变量Cox回归模型来检验年龄差距与全因死亡率、特定病因死亡率和癌症特异性死亡率之间的关联。我们揭示了多器官衰老与可改变因素之间复杂的多样关联网络。所有年龄差距都会使全因死亡率风险增加6%-60%。根据衰老器官的数量,死亡风险从5.54倍到29.18倍不等。特定病因死亡率与某些器官的衰老有关。对于精神疾病死亡率和神经系统死亡率,只有大脑衰老分别显示出显著增加的风险,风险比分别为2.38(每标准差,95%置信区间:2.06-2.74)和1.99(每标准差,95%置信区间:1.84-2.16)。胃的年龄差距也是胃癌的一个特定指标。最终,我们发现一个器官的生物学年龄会选择性地影响其他器官系统的衰老。我们的研究表明,特定器官的加速衰老会增加各种原因导致的死亡风险。这为早期识别高危人群提供了一个潜在工具,为精准医学提供了一种相对客观的方法。