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Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging.
Aging Cell ( IF 8.0 ) Pub Date : 2020-07-30 , DOI: 10.1111/acel.13203
Víctor Fanjul 1, 2, 3 , Inmaculada Jorge 1, 3 , Emilio Camafeita 1, 3 , Álvaro Macías 1, 3 , Cristina González-Gómez 1, 3 , Ana Barettino 1, 3 , Beatriz Dorado 1, 3 , María Jesús Andrés-Manzano 1, 3 , José Rivera-Torres 1, 3 , Jesús Vázquez 1, 3 , Carlos López-Otín 2, 4 , Vicente Andrés 1, 3
Affiliation  

Aging is the main risk factor for cardiovascular and metabolic diseases, which have become a global concern as the world population ages. These diseases and the aging process are exacerbated in Hutchinson–Gilford progeria syndrome (HGPS or progeria). Here, we evaluated the cardiometabolic disease in animal models of premature and normal aging with the aim of identifying alterations that are shared or specific to each condition. Despite differences in body composition and metabolic markers, prematurely and normally aging mice developed heart failure and similar cardiac electrical abnormalities. High‐throughput proteomics of the hearts of progeric and normally aged mice revealed altered protein oxidation and glycation, as well as dysregulated pathways regulating energy metabolism, proteostasis, gene expression, and cardiac muscle contraction. These results were corroborated in the hearts of progeric pigs, underscoring the translational potential of our findings, which could help in the design of strategies to prevent or slow age‐related cardiometabolic disease.

中文翻译:

鉴定小鼠和猪衰老模型中常见的心脏代谢改变和失调途径。

老龄化是心血管和代谢疾病的主要危险因素,随着世界人口老龄化,这些疾病已成为全球关注的问题。这些疾病和衰老过程在哈钦森-吉尔福德早衰症(HGPS 或早衰症)中加剧。在这里,我们在过早和正常衰老的动物模型中评估了心脏代谢疾病,目的是确定每种情况共有或特定的改变。尽管身体成分和代谢标志物存在差异,但过早和正常衰老的小鼠会出现心力衰竭和类似的心脏电异常。早衰和正常衰老小鼠心脏的高通量蛋白质组学揭示了蛋白质氧化和糖化的改变,以及调节能量代谢、蛋白质稳态、基因表达和心肌收缩的失调途径。
更新日期:2020-09-24
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