Open AccessIdentification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging
Author(s) -
Fanjul Víctor,
Jorge Inmaculada,
Camafeita Emilio,
Macías Álvaro,
GonzálezGómez Cristina,
Barettino Ana,
Dorado Beatriz,
AndrésManzano María Jesús,
RiveraTorres José,
Vázquez Jesús,
LópezOtín Carlos,
Andrés Vicente
Publication year - 2020
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13203
Subject(s) - proteostasis , progeria , biology , disease , heart failure , metabolic syndrome , bioinformatics , population , endocrinology , medicine , physiology , genetics , diabetes mellitus , gene , environmental health
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.