ArticleClinical interventions in aging2019
Aged kidneys are refractory to autophagy activation in a rat model of renal ischemia-reperfusion injury.
Article in Clinical interventions in aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 21 citations in OpenAlex.
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Senescence and SASP Are Potential Therapeutic Targets for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- Preserving and rejuvenating old organs for transplantation: novel treatments including the potential of senolytics.Current opinion in organ transplantation · 2022Review
- Acute kidney injury and aging.Pediatric nephrology (Berlin, Germany) · 2021Review
- Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.International journal of molecular medicine · 2021Article
- TUNEL Assay: A Powerful Tool for Kidney Injury Evaluation.International journal of molecular sciences · 2021Review
- Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion-Induced Acute Kidney Injury by Regulating miR-124-3p/MMP2 Axis.BioMed research international · 2021Article
- Article
- Decreased ovarian function and autophagy gene methylation in aging rats.Journal of ovarian research · 2020Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemia-reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Numerous therapeutic approaches for I/R injury have been studied, including autophagy, particularly in animal models of renal I/R injury derived from young or adult animals. However, the precise role of autophagy in renal ischemia-reperfusion in the aged animal model remains unclear. The purpose of this study was to demonstrate whether autophagy has similar effects on renal I/R injury in young and aged rats. MATERIALS AND
methodsAll rats were divided into two age groups (3 months and 24 months) with each group being further divided into four subgroups (sham, I/R, I/R+Rap (rapamycin, an activator of autophagy), I/R+3-MA (3-methyladenine, an inhibitor of autophagy)). The I/R+Rap and I/R+3-MA groups were intraperitoneally injected with rapamycin and 3-MA prior to ischemia. We then measured serum levels of urea nitrogen, creatinine and assessed damage in the renal tissue. Immunohistochemistry was used to assess LC3-II and caspase-3, and Western blotting was used to evaluate the autophagy-related proteins LC3-II, Beclin-1 and P62. Apoptosis and autophagosomes were evaluated by TUNEL and transmission electron microscopy, respectively.
resultsAutophagy was activated in both young and aged rats by I/R and enhanced by rapamycin, although the level of autophagy was lower in the aged groups. In young rats, the activation of autophagy markedly improved renal function, reduced apoptosis in the renal tubular epithelial cells and the injury score in the renal tissue, thereby exerting protective effects on renal I/R injury. However, this level of protection was not present in aged rats.
conclusionOur data indicated that the activation of autophagy was ineffective in aged rat kidneys. These discoveries may have major implications in that severe apoptosis in aged kidneys might be refractory to antiapoptotic effect induced by the activation of autophagy.
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