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Fig. 7

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Song et al., 2026 - Formononetin attenuates glucocorticoid-induced osteoporosis via multiple osteoimmunological pathways: evidence from zebrafish and network pharmacology
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Fig. 7

Schematic illustration of the proposed mechanistic role of FMN in regulating the "inflammation-oxidative stress-bone resorption" axis. (A) Under glucocorticoid-induced osteoporotic conditions, a proposed pathological signaling network involving key targets is depicted. This milieu is characterized by the upregulation of pro-inflammatory and pro-osteoclastogenic factors (e.g., jun, ptgs2 and gsk-3β), alongside the suppression of factors related to growth signaling and calcium homeostasis (e.g., egfr, calm3). (B) FMN treatment counteracts the osteoporotic pathology by restoring the expression of the dysregulated targets, thereby rebalancing bone metabolism. Red/green arrows indicate the regulative direction of gene expression changes (upward for increase, downward for decrease) in response to either pathological induction (A) or therapeutic intervention (B).The figure was designed by the author using BioRender (https://biorender.com) and does not reproduce any published material

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