ArticlePhysiological reports2013
Aldosterone and angiotensin II induce protein aggregation in renal proximal tubules.
Article in Physiological reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- The kidney distal tubule potassium switch, modern diet and hypertension.Nature reviews. Nephrology · 2026Review
- Dopamine D1-like and Angiotensin II Type 1 Receptors Counter-Regulate Autophagy and Cell Proliferation in Rat Embryonic Thoracic Vascular Smooth Muscle Cells.International journal of molecular sciences · 2026Article
- Small bites for big problems: stepwise aggregate degradation by autophagy.Biochemical Society transactions · 2026Review
- Revisiting renin-angiotensin-aldosterone system in aging: translational insights from bench to bedside and back.The Journal of clinical investigation · 2025Review
- Cellular Protein Aggregates: Formation, Biological Effects, and Ways of Elimination.International journal of molecular sciences · 2023Review
- O-Linked β-Frontiers in immunology · 2022Review
- Vascular Stress Signaling in Hypertension.Circulation research · 2021Review
- Peripherally misfolded proteins exacerbate ischemic stroke-induced neuroinflammation and brain injury.Journal of neuroinflammation · 2021Article
- Angiotensin II- and Alzheimer-Type Cardiovascular Aging.Circulation research · 2018Article
- Neo-Epitopes Generated on Hydroxyl Radical Modified GlycatedIgG Have Role in Immunopathology of Diabetes Type 2.PloS one · 2017Article
- Overexpressed cyclophilin B suppresses aldosterone-induced proximal tubular cell injury both in vitro and in vivo.Oncotarget · 2016Article
- Autophagy: a housekeeper in cardiorenal metabolic health and disease.Biochimica et biophysica acta · 2015Review
- Distal renal tubules are deficient in aggresome formation and autophagy upon aldosterone administration.PloS one · 2014Article
Corrections and comments
- Erratum issuedCorrigendum.2014
- Erratum issuedHoorn, Ewout [corrected to Hoorn, Ewout J]
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubules are highly active transporting epithelia and are at risk of protein aggregation due to high protein turnover and/or oxidative stress. We hypothesized that the risk of aggregation was increased upon hormone stimulation and assessed the state of the intracellular protein degradation systems in the kidney from control rats and rats receiving aldosterone or angiotensin II treatment for 7 days. Control rats formed both aggresomes and autophagosomes specifically in the proximal tubules, indicating a need for these structures even under baseline conditions. Fluorescence sorted aggresomes contained various rat keratins known to be expressed in renal tubules as assessed by protein mass spectrometry. Aldosterone administration increased the abundance of the proximal tubular aggresomal protein keratin 5, the ribosomal protein RPL27, ataxin-3, and the chaperone heat shock protein 70-4 with no apparent change in the aggresome-autophagosome markers. Angiotensin II induced aggregation of RPL27 specifically in proximal tubules, again without apparent change in antiaggregating proteins or the aggresome-autophagosome markers. Albumin endocytosis was unaffected by the hormone administration. Taken together, we find that the renal proximal tubules display aggresome formation and autophagy. Despite an increase in aggregation-prone protein load in these tubules during hormone treatment, renal proximal tubules seem to have sufficient capacity for removing protein aggregates from the cells.
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