Sunday, October 19, 2025

Hepatic Deletion of Smad7 in Mouse Leads to Spontaneous Liver Dysfunction and Aggravates Alcoholic Liver Injury

Authors: Lu Zhu, Lingdi Wang, Xiao Wang, Xiaolin Luo, Ling Yang, Rui Zhang, Hongkun Yin, Dong Xie, Yi Pan, Yan Chen

DOI: 10.1371/journal.pone.0017415

Abstract Summary

New research reveals that Smad7, a protein that regulates TGF-β signaling, plays a crucial protective role in liver health. Mice lacking Smad7 in liver cells developed spontaneous liver dysfunction and showed dramatically worsened alcohol-induced liver damage, including increased fat accumulation and inflammation.

Why Brain? 🧠

Study reveals Smad7 protein protects liver function – mice lacking it develop spontaneous liver damage and worse alcohol-induced injury, suggesting new therapeutic targets for liver disease.

The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.

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