ArticleMolecular medicine reports2019
Aldosterone promotes renal interstitial fibrosis via the AIF‑1/AKT/mTOR signaling pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Cinnamaldehyde Attenuates Hyperuricemia-Associated Renal Injury by Modulating Urate Transporters and AIF1- and CMPK2/NLRP3-Related Inflammatory Signaling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- Finerenone in kidney transplantation: an underinvestigated agent: review of available evidence, existing gaps, and future directions.Clinical transplantation and research · 2026Review
- AIF-1 Drives Corneal Neovascularization by Promoting Inflammatory Macrophage Activation via the MAPK and PI3K/AKT/mTOR Signaling Pathways.Investigative ophthalmology & visual science · 2026Article
- The multifaceted role of AIF-1 in metabolic dysregulation: bridging inflammation, insulin resistance, and obesity.Frontiers in endocrinology · 2026Review
- Association of Plasma Aldosterone Concentration With Early Renal Injury Biomarkers in Primary Aldosteronism: A Propensity-Matched Comparative Study.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Mineralocorticoid receptor blockage in kidney transplantation: too much of a good thing or not?International urology and nephrology · 2025Review
- Mechanical regulation of macrophage metabolism by allograft inflammatory factor 1 leads to adverse remodeling after cardiac injury.Nature cardiovascular research · 2025Article
- The Renin-Angiotensin-Aldosterone System Regulates Sarcoidosis Granulomatous Inflammation.American journal of respiratory and critical care medicine · 2024Article
- LincRNA-p21/AIF-1/CMPK2/NLRP3 pathway promoted inflammation, autophagy and apoptosis of human tubular epithelial cell induced by urate via exosomes.Scientific reports · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- Cellular crosstalk of mesangial cells and tubular epithelial cells in diabetic kidney disease.Cell communication and signaling : CCS · 2023Review
- Review
- Zinc oxide nanoparticles and spironolactone-enhanced Nrf2/HO-1 pathway and inhibited Wnt/β-catenin pathway in adenine-induced nephrotoxicity in rats.Redox report : communications in free radical research · 2022Article
- ICAM-1 related long noncoding RNA is associated with progression of IgA nephropathy and fibrotic changes in proximal tubular cells.Scientific reports · 2022Article
- AIF-1, a potential biomarker of aggressive tumor behavior in patients with non-small cell lung cancer.PloS one · 2022Article
- AKT/foxo3a signal pathway mediates the protective mechanism of resveratrol on renal interstitial fibrosis and oxidative stress in rats with unilateral ureteral obstruction.American journal of translational research · 2022Article
- Aldosterone Negatively Regulates Nrf2 Activity: An Additional Mechanism Contributing to Oxidative Stress and Vascular Dysfunction by Aldosterone.International journal of molecular sciences · 2021Article
- 1,25-(OH)The Journal of international medical research · 2021Article
- Huoxue Jiedu Huayu Formula Alleviates Cell Pyroptosis in Contralateral Kidneys of 6-Month-Old UUO Rats through the NLRP3/Caspase-1/IL-1Evidence-based complementary and alternative medicine : eCAM · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of studies have shown that aldosterone serves an important role in promoting renal interstitial fibrosis, although the specific mechanism remains to be elucidated. A previous study revealed that the fibrotic effect of aldosterone was associated with the expression of allograft inflammatory factor 1 (AIF‑1) in RAW264.7 macrophage cells, in a time‑ and concentration‑dependent manner. However, the exact mechanism through which aldosterone promotes renal interstitial fibrosis remains unknown. In the present study, the effects of aldosterone on renal inflammatory cell infiltration, collagen deposition and the expression levels of AIF‑1, phosphatidylinositol 3‑kinase (PI3K), AKT serine/threonine kinase (AKT), mammalian target of rapamycin (mTOR), the oxidative stress factor NADPH oxidase 2 (NOX2) and nuclear transcription factor erythroid‑related factor 2 (Nrf2) were assessed in normal rats, rats treated with aldosterone, rats treated with aldosterone and spironolactone and those treated with spironolactone only (used as the control). The effect of aldosterone on these factors was also investigated in the renal interstitium of unilateral ureteral obstruction (UUO) rats. Additionally, the AIF‑1 gene was overexpressed and knocked down in macrophage RAW264.7 cells, and the effects of aldosterone on PI3K, AKT, mTOR, NOX2 and Nrf2 were subsequently investigated. The results showed that aldosterone promoted inflammatory cell infiltration, collagen deposition and the expression of AIF‑1, PI3K, AKT, mTOR and NOX2, but inhibited the expression of Nrf2. In the UUO rats, aldosterone also promoted renal interstitial inflammatory cell infiltration, collagen deposition and the expression of AIF‑1, NOX2, PI3K, AKT and mTOR, whereas the expression of Nrf2 was downregulated by aldosterone compared with that in the UUO‑only group; the influence of aldosterone was counteracted by spironolactone in the normal and UUO rats. In vitro, aldosterone upregulated the expression levels of AKT, mTOR, NOX2 and Nrf2 in RAW264.7 cells compared with those in untreated cells. Suppressing the expression of AIF‑1 inhibited the effects of aldosterone, whereas the overexpression of AIF‑1 enhanced these effects in RAW264.7 cells. These findings indicated that aldosterone promoted renal interstitial fibrosis by upregulating the expression of AIF‑1 and that the specific mechanism may involve AKT/mTOR and oxidative stress signaling.
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