ArticleThe Journal of clinical investigation2016
p66Shc regulates renal vascular tone in hypertension-induced nephropathy.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- The role of C-C motif chemokine ligand 2 in the preservation of myogenic tone in the kidney microvasculature of Dahl Salt-Sensitive rats.Kidney international · 2026Article
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Multidimensional Mechanisms of Hypertension and Advances in Diagnosis and Integrated TCM-Based Treatment: A Review.International journal of general medicine · 2026Review
- Protective Role of p66Shc Deletion in Physiological Renal Aging: Effects on G Protein-Coupled Receptor 124 Expression and Associated Cellular Senescence.International journal of molecular sciences · 2025Article
- Non-Ser36 phosphorylated p66Shc inhibits TRPC-dependent and TRPC-independent calcium influx in vascular smooth muscle cells.Biochemical and biophysical research communications · 2025Article
- Is It Time to Abandon the Kidney-Centered View on the Origin of Primary Hypertension?Hypertension (Dallas, Tex. : 1979) · 2025Review
- Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage.International journal of molecular sciences · 2025Review
- Prevention of hypertension-induced renal vascular dysfunction through a p66Shc-targeted mechanism.American journal of physiology. Renal physiology · 2025Article
- Targeting p66Shc to restore KFrontiers in physiology · 2025Article
- PAR1-mediated Non-periodical Synchronized Calcium Oscillations in Human Mesangial Cells.Function (Oxford, England) · 2024Article
- β-Arrestin pathway activation by selective ATR1 agonism promotes calcium influx in podocytes, leading to glomerular damage.Clinical science (London, England : 1979) · 2023Article
- Autoregulatory mission impossible: when afferent arterioles lose contractility.Kidney international · 2023Article
- Matrix metalloproteinase-9 regulates afferent arteriolar remodeling and function in hypertension-induced kidney disease.Kidney international · 2023Article
- Epigenetic Signatures in Arterial Hypertension: Focus on the Microvasculature.International journal of molecular sciences · 2023Review
- New developments in translational microcirculatory research.American journal of physiology. Heart and circulatory physiology · 2022Review
- p66Shc signaling does not contribute to tubular damage induced by renal ischemia-reperfusion injury in rat.Biochemical and biophysical research communications · 2022Article
- Modulation of p66Shc impairs cerebrovascular myogenic tone in low renin but not low nitric oxide models of systemic hypertension.American journal of physiology. Heart and circulatory physiology · 2021Article
- p66Shc-mediated hydrogen peroxide production impairs nephrogenesis causing reduction of number of glomeruli.Life sciences · 2021Article
- Double p52Shc/p46Shc Rat Knockout Demonstrates Severe Gait Abnormalities Accompanied by Dilated Cardiomyopathy.International journal of molecular sciences · 2021Article
- Piperazine ferulate attenuates high glucose‑induced mesangial cell injury via the regulation of p66Molecular medicine reports · 2021Article
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14 authors at 1 institution in 1 country.
Funding
Abstract
Renal preglomerular arterioles regulate vascular tone to ensure a large pressure gradient over short distances, a function that is extremely important for maintaining renal microcirculation. Regulation of renal microvascular tone is impaired in salt-sensitive (SS) hypertension-induced nephropathy, but the molecular mechanisms contributing to this impairment remain elusive. Here, we assessed the contribution of the SH2 adaptor protein p66Shc (encoded by Shc1) in regulating renal vascular tone and the development of renal vascular dysfunction associated with hypertension-induced nephropathy. We generated a panel of mutant rat strains in which specific modifications of Shc1 were introduced into the Dahl SS rats. In SS rats, overexpression of p66Shc was linked to increased renal damage. Conversely, deletion of p66Shc from these rats restored the myogenic responsiveness of renal preglomerular arterioles ex vivo and promoted cellular contraction in primary vascular smooth muscle cells (SMCs) that were isolated from renal vessels. In primary SMCs, p66Shc restricted the activation of transient receptor potential cation channels to attenuate cytosolic Ca2+ influx, implicating a mechanism by which overexpression of p66Shc impairs renal vascular reactivity. These results establish the adaptor protein p66Shc as a regulator of renal vascular tone and a driver of impaired renal vascular function in hypertension-induced nephropathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.