Nutrition, metabolism, and cardiovascular diseases : NMCD · 2025
Maternal obesity negatively impacts cardiac progenitor cell survival in heart adulthood offspring.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Andrade Daniela C, Gaetani Bruna, Moura Sara, de Carvalho Simone N, Thole Alessandra A, Cortez Erika
Аннотация
BACKGROUND AND AIM: Maternal obesity has been related to offspring predisposition to cardiometabolic disease development throughout life. Thus, this study aimed to analyze the impact of maternal obesity on cardiac progenitor cells and cardiometabolic disease of adult offspring.
METHODS AND RESULTS: The litter size reduction experimental model was used to induce obesity in female Swiss mice. Small Litter Dam (SLD-F1) and Normal Litter Dam (NLD-F1) were crossed with healthy male mice, and their offspring were followed up until 90 days old when they were euthanized. Adult offspring of obese dams (SLD-F2) had increased body mass, Lee Index and fat deposits. Heart analysis demonstrated cardiac hypertrophy, fibrosis, oxidative stress, increased cardiac mast cell number, decreased cellular proliferation, increased proinflammatory cytokines, and mitochondrial dynamic impairment. These cardiometabolic modifications were accompanied by reduced c-kit+ and Sca-1+ cardiac progenitor cell (CPC) populations and impaired CPC differentiation into new cardiomyocytes.
CONCLUSIONS: In conclusion, Obese mother-offspring developed cardiometabolic changes in adulthood that negatively impacted the CPC niches and, consequently, the formation of new cardiomyocytes. This process seems to be an essential mechanism involved in the pathophysiology of the disease, impairing cardiac homeostasis.
METHODS AND RESULTS: The litter size reduction experimental model was used to induce obesity in female Swiss mice. Small Litter Dam (SLD-F1) and Normal Litter Dam (NLD-F1) were crossed with healthy male mice, and their offspring were followed up until 90 days old when they were euthanized. Adult offspring of obese dams (SLD-F2) had increased body mass, Lee Index and fat deposits. Heart analysis demonstrated cardiac hypertrophy, fibrosis, oxidative stress, increased cardiac mast cell number, decreased cellular proliferation, increased proinflammatory cytokines, and mitochondrial dynamic impairment. These cardiometabolic modifications were accompanied by reduced c-kit+ and Sca-1+ cardiac progenitor cell (CPC) populations and impaired CPC differentiation into new cardiomyocytes.
CONCLUSIONS: In conclusion, Obese mother-offspring developed cardiometabolic changes in adulthood that negatively impacted the CPC niches and, consequently, the formation of new cardiomyocytes. This process seems to be an essential mechanism involved in the pathophysiology of the disease, impairing cardiac homeostasis.
Предметные рубрики MeSH
AnimalsFemalePregnancyMalePregnancy in ObesityMyocytes, CardiacPrenatal Exposure Delayed EffectsDisease Models, AnimalOxidative StressCell SurvivalCell ProliferationCell DifferentiationInflammation MediatorsMitochondria, HeartMiceFibrosisCardiomegalyAge FactorsStem Cell NicheStem CellsCytokinesAdiposityLitter Size