BMAL1 regulates tubular epithelial-derived exosomal miR-27a-3p to inhibit macrophage–myofibroblast transition and alleviate ischemia/reperfusion-induced renal fibrosis
Wu Chen, Sheng Zhao, Songyuan Yang, Weimin Yu, Ting Rao, Xiangjun Zhou, Yuan Ruan, Fan Zou, Fan Cheng, Wei Li · 2026
Read BMAL1 regulates tubular epithelial-derived exosomal miR-27a-3p to inhibit macrophage–myofibroblast transition and alleviate ischemia/reperfusion-induced renal fibrosis by Wu Chen, Sheng Zhao, Songyuan Yang, Weimin Yu, Ting Rao, Xiangjun Zhou, Yuan Ruan, Fan Zou, Fan Cheng, Wei Li (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13232619.txt.
Description
Wu Chen and colleagues report a two thousand twenty-six study of the body-clock gene BMAL1 protecting kidneys after blood-flow injury and reperfusion. Restored flow after blockage scars kidneys through progressive fibrosis. Immune macrophages can convert into scar-forming cells, worsening the damage over time.
Kidney-specific BMAL1 boosting in mice reduced scarring after the injury. The gene raised a small RNA shipped in tiny exosome packages from tubule cells. That cargo blocked a growth signal inside macrophages, stopping their conversion into scar cells. Cell and animal experiments confirmed each link. Clock biology thus offers a fresh anti-fibrosis lever for injured kidneys.
Catalog record
| CREATOR | Wu Chen, Sheng Zhao, Songyuan Yang, Weimin Yu, Ting Rao, Xiangjun Zhou, Yuan Ruan, Fan Zou, Fan Cheng, Wei Li |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 40 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |