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Updated: May 13, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
Published on: November 21, 2025
Basic helix-loop-helix transcriptional factor MyoR regulates BMP-7 in acute kidney injury
Nozomu Kamiura1, Junichi Hirahashi, Yumi Matsuzaki
1Department of Advanced Nephrology and Regenerative Medicine, University of Tokyo, Tokyo, Japan.
Abstract:
MyoR was originally identified as a transcriptional repressor in embryonic skeletal muscle precursors, but its function in adult kidney has not been clarified. In this study, we tried to clarify the functional role of MyoR using MyoR(-/-) mice. Cisplatin induced a significantly higher degree of severe renal dysfunction, tubular injury, and mortality in MyoR(-/-) mice than in wild-type mice. The injection of cisplatin significantly increased the number of apoptotic cells in the kidney tissues of MyoR(-/-) mice, compared with that in wild-type mice. To clarify the mechanism of severe cisplatin-induced damage and apoptosis in MyoR(-/-) mice, we focused on the p53 signaling pathway and bone morphogenic protein-7 (BMP-7). Treatment with cisplatin significantly activated p53 signaling in cultured renal proximal tubular epithelial cells (RTECs) in both wild-type and MyoR(-/-) mice, but no significant difference between the groups was observed. The injection of cisplatin significantly increased the expression of BMP-7 in the kidney tissues of wild-type mice, but no increase was observed in the MyoR(-/-) mice. Treatment with cisplatin significantly increased the expression of BMP-7 in cultured RTECs from wild-type mice but not in those from MyoR(-/-) mice. Moreover, treatment with recombinant BMP-7 rescued the cisplatin-induced apoptosis in RTECs from MyoR(-/-) mice. Taken together, our results demonstrate a new protective role of MyoR in adult kidneys that acts through the regulation of BMP-7.
Insights
MyoR plays a protective role in adult kidneys. Loss of MyoR exacerbates cisplatin-induced kidney injury by impairing bone morphogenic protein-7 (BMP-7) expression and increasing apoptosis.
Area of Science:
- Nephrology
- Molecular Biology
- Toxicology
Background:
- MyoR, a transcriptional repressor, has an unclear function in adult kidneys.
- Understanding MyoR's role is crucial for kidney protection.
Purpose of the Study:
- To elucidate the functional role of MyoR in adult kidney injury.
- To investigate the mechanism underlying MyoR's protective effects against cisplatin-induced nephrotoxicity.
Main Methods:
- Utilized MyoR knockout (MyoR(-/-)) and wild-type mice.
- Administered cisplatin to induce kidney injury.
- Analyzed renal dysfunction, tubular injury, mortality, apoptosis, p53 signaling, and BMP-7 expression.
- Utilized cultured renal proximal tubular epithelial cells (RTECs).
Main Results:
- MyoR(-/-) mice exhibited increased susceptibility to cisplatin-induced renal dysfunction, tubular injury, and mortality.
- Cisplatin treatment led to significantly higher apoptosis in MyoR(-/-) kidneys.
- MyoR deficiency impaired the cisplatin-induced increase in bone morphogenic protein-7 (BMP-7) expression.
- BMP-7 administration rescued cisplatin-induced apoptosis in MyoR(-/-) RTECs.
Conclusions:
- MyoR plays a novel protective role in adult kidneys against cisplatin-induced injury.
- MyoR's protective mechanism involves the regulation of BMP-7 expression.
- Targeting MyoR or BMP-7 may offer therapeutic strategies for nephroprotection.
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