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Published on: February 20, 2019
Early-life atherogenesis: Mechanistic pathways, risk architecture, and clinical implications in pediatric populations
Citlaly Natali de la Torre-Sosa1, Rebeca López-Marure2, Héctor Ochoa-Díaz-López3
1Departamento de Salud, El Colegio de la Frontera Sur (ECOSUR), Unidad Villahermosa, Carretera a Reforma Km. 15.5 s/n, Ranchería Guineo 2da Sección, CP 86280, Villahermosa, Tabasco, Mexico.
Abstract:
Atherosclerosis is now recognized as a long-term biological process whose origins may be established early in life, well before the clinical expression of cardiovascular disease. The increasing prevalence of pediatric obesity, insulin resistance, sedentary behavior, and unhealthy dietary patterns has intensified interest in understanding how vascular risk is shaped from childhood onward. This narrative review examines early-life atherogenesis in pediatric populations from mechanistic, clinical, and preventive perspectives, with emphasis on cardiometabolic risk factors, endothelial dysfunction, vascular inflammation, and potential biomarkers of subclinical vascular injury. A narrative synthesis of current evidence was conducted to integrate mechanistic, clinical, and preventive aspects of pediatric atherogenesis, focusing on biological pathways, developmental determinants, lifestyle-related exposures, and emerging tools for early risk stratification. Sustained exposure to adverse cardiometabolic factors during childhood and adolescence may promote subclinical vascular alterations and establish risk trajectories that persist into adulthood. This process involves the interaction of atherogenic dyslipidemia, oxidative stress, chronic low-grade inflammation, immune activation, endothelial dysfunction, and vascular remodeling. Circulating biomarkers of endothelial activation and vascular inflammation may serve as early indicators of subclinical injury and provide complementary information for identifying children with increased cardiometabolic vulnerability. Genetic susceptibility, pubertal development, sex-related differences, socioeconomic conditions, and lifestyle-related factors further modulate the expression and severity of risk. Early identification of children with unfavorable cardiometabolic profiles requires the integration of conventional clinical assessment with biomarkers, derived lipid parameters, and complementary stratification tools that still require further pediatric validation. Understanding pediatric atherogenesis as an integrated process shaped by biology, development, and environment may help guide more timely strategies for prevention, follow-up, and intervention aimed at reducing future cardiovascular burden.
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