Type II alveolar epithelial cell-specific CAP1 loss is associated with spontaneous pulmonary fibrosis and altered complement 5 signaling
Bingbing Wang, Yunlu Gu, Jushan Zhang, Amanguli Tuerhong, Yujie Zhu, Binay Kumar Shah, Changhui Wang, Shuanshuan Xie · 2026
Read Type II alveolar epithelial cell-specific CAP1 loss is associated with spontaneous pulmonary fibrosis and altered complement 5 signaling by Bingbing Wang, Yunlu Gu, Jushan Zhang, Amanguli Tuerhong, Yujie Zhu, Binay Kumar Shah, Changhui Wang, Shuanshuan Xie (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-13483859.txt.
Description
Wang and colleagues removed a little-studied protein from one lung cell type in mice and watched lung scarring develop on its own. The protein, CAP1, was deleted only in type II alveolar cells, the cells that coat air sacs and repair them after injury. Their 2026 study then tracked survival, breathing mechanics, tissue structure, and gene activity in the altered lungs.
Mice lacking CAP1 died sooner than their normal littermates in the reported follow-up. A subset declined visibly, losing weight and activity while lung stiffness rose and breathing capacity fell. Tissue sections showed scarred, disorganized air sacs with immune cells crowding in, and standard fibrosis scores climbed. Gene scans highlighted scar-building pathways and changed signaling from complement 5, part of the immune alarm system. Wang proposes CAP1 helps keep air-sac cells stable.
Catalog record
| CREATOR | Bingbing Wang, Yunlu Gu, Jushan Zhang, Amanguli Tuerhong, Yujie Zhu, Binay Kumar Shah, Changhui Wang, Shuanshuan Xie |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 48 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |