ArticleFrontiers in physiology2020
Renal Programming by Transient Postnatal Overfeeding: The Role of Senescence Pathways.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Effect of Protein Intake Early in Life on Kidney Volume and Blood Pressure at 11 Years of Age.Nutrients · 2023Trial
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Geroprotective effects of GdVOBiogerontology · 2024Article
- High Amino Acid Intake in Early Life Is Associated With Systolic but Not Diastolic Arterial Hypertension at 5 Years of Age in Children Born Very Preterm.Journal of the American Heart Association · 2024Article
- Nutrition and Developmental Origins of Kidney Disease.Nutrients · 2023Review
- The reduced number of nephrons with shortening renal tubules in mouse postnatal adverse environment.Pediatric research · 2023Article
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Exploring the Critical Components and Therapeutic Mechanisms ofFrontiers in pharmacology · 2021Article
- Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEarly nutrition influences the risk of chronic kidney diseases (CKDs) development in adulthood. Mechanisms underlying the early programming of altered renal function remain incompletely understood. This study aims at characterizing the role of cell senescence pathways in early programming of CKD after transient postnatal overfeeding. MATERIALS AND
methodsReduced litters of 3 mice pups and standard litters of 9 mice pups were obtained to induce overfed animals during lactation and control animals, respectively. Animals were sacrificed at 24 days (weaning) or at 7 months of life (adulthood). Body weight, blood pressure, kidney weight, and glomerular count were assessed in both groups. Senescence pathways were investigated using β-Galactosidase staining and Western blotting of P16, P21, P53, P-Rb/Rb, and Sirtuin 1 (Sirt1) proteins.
resultsEarly overfed animals had a higher body weight, a higher blood pressure at adulthood, and a higher glomerular number endowment compared to the control group. A higher β-Galactosidase activity, a significant increase in P53 protein expression (
conclusionEarly postnatal overfeeding by litter size reduction is associated with increased expression of factors involved in cellular senescence pathways, and decreased expression of Sirt 1 in the mouse kidney at weaning. These alterations may contribute to CKD programming after early postnatal overfeeding.
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