ArticleAmerican journal of physiology. Renal physiology2025
Prevention of hypertension-induced renal vascular dysfunction through a p66Shc-targeted mechanism.
Article in American journal of physiology. Renal physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Prevalence and risk factors of acute kidney injury in adults with obesity undergoing bariatric surgery: a systematic review and meta-analysis.Wideochirurgia i inne techniki maloinwazyjne = Videosurgery and other miniinvasive techniques · 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
- Targeting p66Shc to restore KFrontiers in physiology · 2025Article
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7 authors.
Funding
Abstract
Renal microvascular injury occurs in most patients with hypertension-induced nephropathy (HN). We have shown that overexpression of adaptor protein p66Shc is implicated in the loss of renal microvascular reactivity in hypertensive rats. Since sulfur heteroarotinoid A2 (SHetA2) modulates p66Shc, we tested whether SHetA2 would restore renal microvascular reactivity and mitigate kidney injury in a rat HN model. Dahl salt sensitive (SS) and p66Shc knockout (p66Shc-KO) rats were used in a well-established rat model of HN, characterized by severe renal vascular dysfunction. SHetA2 was either added acutely to isolated rat afferent arterioles or chronically administrated to rats during HN development. The ability of SHetA2 treatment to restore afferent arteriolar contraction in response to increased perfusion pressure or ATP was evaluated using the perfused juxtamedullary nephron preparation. The progression of renal damage was evaluated by measuring urinary protein excretion and conducting analysis of glomerular injury. Comparison of renal microvascular responses to perfusion pressure in p66Shc-KO rats and parental SS rats, in the presence and absence of acute preincubation with SHetA2, revealed a dose-dependent ability of SHetA2 to restore renal microvascular reactivity in SS rats with little effect upon p66Shc knockouts. Moreover, chronic treatment with SHetA2 prevented loss of renal microvascular responses and decline in renal function. SHetA2 was more potent and effective in males compared with females. Targeting p66Shc with SHetA2 diminishes renal damage and restores renal afferent arteriolar reactivity caused by hypertension. These results justify further translation of these findings to develop SHetA2 for prevention and treatment of hypertension-induced kidney damage.
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