Abstract：
Travel to space has overcome unprecedent technological challenges and this has resulted in transfer of these technological results on Earth to better our lives. Health technology, medical devices, and research advancements in human biology are the first beneficiaries of this transfer. The real breakthrough came with the International Space Station, which endorsed multidisciplinary international scientific collaborations and boosted the research on pathophysiological adaptation of astronauts to life on space. These studies evidenced that life in space appeared to have exposed the astronauts to an accelerated aging-related pathophysiological dysregulation across multiple systems. In this review we emphasize the interaction between several biomarkers and their alteration in concentrations/expression/function by space stress factors. These altered interactions, suggest that different biochemical and hormonal factors, and cell signals, contribute to a complex network of pathophysiological mechanisms, orchestrating the homeostatic dysregulation of various organs/metabolic pathways. The main effects of space travel on altering cell organelles biology, ultrastructure, and cross-talk, have been observed in cell aging as well as in the disruption of metabolic pathways, which are also the causal factor of rare inherited metabolic disorders, one of the major pediatric health issue. The pathophysiologic breakthrough from space research could allow the development of precision health both on Earth and Space by promoting the validation of improved biomarker-based risk scores and the exploration of new pathophysiologic hypotheses and therapeutic targets. Nonstandard abbreviations: International Space Station (ISS), Artificial Intelligence (AI), European Space Agency (ESA), National Aeronautics and Space Agency (NASA), Low Earth Orbit (LEO), high sensitive troponin (hs-cTn), high sensitive troponin I (hs-cTn I), high sensitive troponin T, Brain Natriuretic Peptide (BNP), N terminal Brain Natriuretic Peptide (NT-BNP), cardiovascular disease (CVD), parathyroid hormone (PTH), urinary hydroxyproline (uHP), urinary C- and N-terminal telopeptides (uCTX and uNTX), pyridinoline (PYD), deoxypyridinoline (DPD), half-time (HF), serum Bone Alkaline Phosphatase (sBSAP), serum Alkaline Phosphatase (sAP), Carboxy-terminal Propeptide of Type 1 Procollagen (P1CP), serum Osteocalcin (sOC)), advanced glycation end products (AGEs), glycated hemoglobin A1c (HbA1c), Insulin-like growth factor 1 (IGF1), Growth Hormone (GH), amino acid (AA), β-hydroxy-β methyl butyrate (HMB), maple syrup urine disease (MSUD), non-communicable diseases (NCDs).
摘要：
太空旅行克服了前所未有的技术挑战，这导致了这些技术成果在地球上的转移，以改善我们的生活。卫生技术,医疗器械,人类生物学的研究进展是这一转移的第一个受益者。真正的突破来自国际空间站，它支持多学科的国际科学合作，并促进了宇航员对太空生活的病理生理适应的研究。这些研究表明，太空中的生命似乎使宇航员经历了多个系统中与衰老相关的加速病理生理失调。在这篇综述中，我们强调了几种生物标志物之间的相互作用及其通过空间应激因子在浓度/表达/功能方面的变化。这些改变的相互作用，表明不同的生化和激素因素，和细胞信号，有助于病理生理机制的复杂网络，协调各种器官/代谢途径的稳态失调。太空旅行对改变细胞器生物学的主要影响，超微结构，和相声,已经在细胞衰老以及代谢途径的破坏中观察到，这也是罕见遗传代谢紊乱的原因，主要的儿科健康问题之一。太空研究的病理生理学突破可以通过促进对改进的基于生物标志物的风险评分的验证以及对新的病理生理学假设和治疗目标的探索，从而在地球和太空上发展精确的健康。非标准缩写：国际空间站（ISS），人工智能(AI),欧洲航天局（ESA）美国国家航空航天局(NASA)低地球轨道(LEO),高敏肌钙蛋白(hs-cTn)，高敏肌钙蛋白I(hs-cTnI)，高敏肌钙蛋白T,脑钠肽(BNP),N末端脑钠肽(NT-BNP),心血管疾病（CVD），甲状旁腺激素（PTH），尿羟脯氨酸（uHP），尿C-和N-末端端肽（uCTX和uNTX），吡啶啉(PYD),脱氧吡啶啉（DPD），半时(HF),血清骨碱性磷酸酶（sBSAP），血清碱性磷酸酶（sAP），1型前胶原（P1CP）的羧基末端前肽，血清骨钙蛋白（sOC）），糖基化终产物（AGEs），糖化血红蛋白A1c（HbA1c），胰岛素样生长因子1(IGF1),生长激素(GH),氨基酸(AA),β-羟基-β-甲基丁酸酯(HMB),枫糖浆尿病（MSUD），非传染性疾病。
