ArticleOxidative medicine and cellular longevity2017
Histopathological Changes in the Kidney following Congestive Heart Failure by Volume Overload in Rats.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Uric Acid-Degrading Lacticaseibacillus paracasei CPU202306 Ameliorates Hyperuricemia by Regulating Uric Acid Metabolism and Intestinal Microecology in Mice.Probiotics and antimicrobial proteins · 2026Article
- Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022Review
- Chronic Naltrexone Therapy Is Associated with Improved Cardiac Function in Volume Overloaded Rats.Cardiovascular drugs and therapy · 2021Article
- Adaptive Autophagy Offers Cardiorenal Protection in Rats with Acute Myocardial Infarction.Cardiology research and practice · 2020Article
- Ellagic acid ameliorates cisplatin toxicity in chemically induced colon carcinogenesis.Molecular and cellular biochemistry · 2019Article
- Genipin alleviates vascular hyperpermeability following hemorrhagic shock by up-regulation of SIRT3/autophagy.Cell death discovery · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study investigated histopathological changes and apoptotic factors that may be involved in the renal damage caused by congestive heart failure in a rat model of infrarenal aortocaval fistula (ACF).
methodsHeart failure was induced using a modified approach of ACF in male Wistar rats. Sham-operated controls and ACF rats were characterized by their morphometric and hemodynamic parameters and investigated for their histopathological, ultrastructural, and apoptotic factor changes in the kidney.
resultsACF-induced heart failure is associated with histopathological signs of congestion and glomerular and tubular atrophy, as well as nuclear and cellular degeneration in the kidney. In parallel, overexpression of proapoptotic Bax protein, release of cytochrome C from the outer mitochondrial membrane into cell cytoplasm, and nuclear transfer of activated caspase 3 indicate apoptotic events. This was confirmed by electron microscopic findings of apoptotic signs in the kidney such as swollen mitochondria and degenerated nuclei in renal tubular cells.
conclusionsThis study provides morphological evidence of renal injury during heart failure which may be due to caspase-mediated apoptosis via overexpression of proapoptotic Bax protein, subsequent mitochondrial cytochrome C release, and final nuclear transfer of activated caspase 3, supporting the notion of a cardiorenal syndrome.
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