ArticleJournal of inflammation research2021
Maternal High-Fat Diet Programs Renal Peroxisomes and Activates NLRP3 Inflammasome-Mediated Pyroptosis in the Rat Fetus.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Obesity-associated unfolded protein response, oxidative stress, and NRF2 signaling.International journal of obesity (2005) · 2026Review
- Impact of diet and exercise in growth restricted female rats on nephron endowment in male fetuses.Experimental physiology · 2026Article
- Developmental Programming of Kidney Disease Across the Life Course: A Narrative Review Focused on Inflammation.International journal of molecular sciences · 2026Review
- A role for the antioxidants coenzyme Q10 and pyrroloquinoline quinone in mitigating obesity-associated reproductive dysfunction†.Biology of reproduction · 2026Review
- Obesity in reproduction: Mechanisms from fertilization to post‑uterine development (Review).International journal of molecular medicine · 2025Review
- Article
- Translational strategies to uncover the etiology of congenital anomalies of the kidney and urinary tract.Pediatric nephrology (Berlin, Germany) · 2025Review
- The role of pyroptosis in the occurrence and development of pregnancy-related diseases.Frontiers in immunology · 2024Review
- Pyrroloquinoline quinone inhibits PCSK9-NLRP3 mediated pyroptosis of Leydig cells in obese mice.Cell death & disease · 2023Article
- Pyrroloquinoline-quinone to reduce fat accumulation and ameliorate obesity progression.Frontiers in molecular biosciences · 2023Review
- Programming by maternal obesity: a pathway to poor cardiometabolic health in the offspring.The Proceedings of the Nutrition Society · 2022Review
- Diet Modification before or during Pregnancy on Maternal and Foetal Outcomes in Rodent Models of Maternal Obesity.Nutrients · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMaternal obesity impairs kidney development and function of the offspring and leads to a greater risk of kidney disease in adulthood. The present study aimed to investigate the link between peroxisomes, oxidative stress (OS), and inflammasomes in the fetal kidney of maternal obesity rats and to explore the potential therapeutic effects of the antioxidant pyrroloquinoline quinone (PQQ).
methodsMaternal obesity rats were developed by administration of a high fat diet plus supplementation with PQQ (40 mg/kg body weight) as a potential therapy. Renal histology was observed by Periodic Acid-Schiff staining. The expression profiles of peroxins, fatty acid β-oxidation enzymes, antioxidants, and the regulators of the unfolded protein response (UPR) pathway and NLRP3 inflammasome were analyzed in the kidneys and tubular epithelial cells (TECs) from near-term fetuses (embryonic day 20).
resultsThe present work revealed that: 1) a maternal high fat diet (MHF) led to higher blood pressure in adult offspring; 2) MHF led to downregulation of peroxisome markers PEX3 and 14 in fetal kidneys; 3) the antioxidant SOD2 and catalase were decreased, and oxidative stress marker Ephx2 was increased; 4) MHF-induced activation of the UPR pathway; 5) the KEAP1-NRF2 pathway was activated; 6) activation of the NLRP3 inflammasome led to secretion of pro-inflammation factors; 7) in TECs, the changes in PEXs and NLRP3 are similar to tissues, but UPR and NRF2 pathways showed opposite trends; 8) and the antioxidant PQQ alleviated maternal lipotoxicity by decreasing ROS levels and inhibiting activation of ER stress and inflammasome in fetal kidney.
conclusionA maternal high fat diet decreased the number of peroxisomes, subsequently activated OS and inflammasomes, resulting in pyroptosis and apoptosis in fetal kidney. The antioxidant PQQ served a protective role against the effects of lipotoxicity on kidney programming and, thus, is a potential candidate to prevent maternal obesity-induced renal programming.
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