Unraveling the mechanisms of nicotine-induced osteoporosis via network toxicology, bioinformatics, and molecular docking.

ABSTRACT:

Introduction

Osteoporosis (OP) is linked to smoking. Nicotine may disrupt bone homeostasis through various pathways, but its molecular mechanisms are unclear. This study aims to explore the molecular networks and key regulatory factors underlying nicotine-induced OP.

Methods

Nicotine toxicity was assessed via ProTox-3.0, with its Simplified Molecular Input Line Entry System (SMILES) structure retrieved from PubChem. Potential targets were predicted using five databases, including SuperPred. OP-related gene data (GSE56815) were extracted from Gene Expression Omnibus (GEO) and combined with GeneCards and Comparative Toxicogenomics Database (CTD) for target screening. Overlapping genes were identified by Venn diagram analysis, followed by protein-protein interaction (PPI) netwo

SUBMITTER: Xu S 

PROVIDER: S-EPMC12817853 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature