ArticleInternational journal of molecular sciences2023
Perinatal Obesity Sensitizes for Premature Kidney Aging Signaling.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Genetic association of immunosenescence to immune decline.Immunogenetics · 2026Review
- Lipid Metabolism and Obesity in Early Life: Drivers of Chronic Lung Disease From Development to Adulthood.Molecular nutrition & food research · 2026Review
- p16INK4a Deletion Alleviated Obesity-Associated Kidney Fibrosis by Regulating Metabolic Reprogramming and the Inflammasome Pathway.Journal of cellular and molecular medicine · 2025Article
- Minoxidil and nebivolol restore aortic elastic fiber homeostasis in diabetic mice via potassium channel activation.Frontiers in physiology · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Chronic Kidney Disease (CKD), a global health burden, is strongly associated with age-related renal function decline, hypertension, and diabetes, which are all frequent consequences of obesity. Despite extensive studies, the mechanisms determining susceptibility to CKD remain insufficiently understood. Clinical evidence together with prior studies from our group showed that perinatal metabolic disorders after intrauterine growth restriction or maternal obesity adversely affect kidney structure and function throughout life. Since obesity and aging processes converge in similar pathways we tested if perinatal obesity caused by high-fat diet (HFD)-fed dams sensitizes aging-associated mechanisms in kidneys of newborn mice. The results showed a marked increase of γH2AX-positive cells with elevated 8-Oxo-dG (RNA/DNA damage), both indicative of DNA damage response and oxidative stress. Using unbiased comprehensive transcriptomics we identified compartment-specific differentially-regulated signaling pathways in kidneys after perinatal obesity. Comparison of these data to transcriptomic data of naturally aged kidneys and prematurely aged kidneys of genetic modified mice with a hypomorphic allele of
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