Evidence map›Paper›PMID 42491154›Full record

ArticleAmerican journal of translational research2026

Psoralen regulates bone degenerative diseases by inhibiting APP phosphorylation to regulate MAPK and STAT3 signaling.

Youji Jia, Wei Yan, Tao Liu, Yong Xu, Zhongwei Li, Xiaobing Xi

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Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Youji JiaDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Wei YanDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Tao LiuDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Yong XuDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Zhongwei LiDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Xiaobing XiDepartment of Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoralen can modulate bone metabolism pathways. This study investigated its effects on bone degenerative diseases, amyloid precursor protein (APP) phosphorylation, and the related pathways.

methodsThe Aβ40/Aβ42 levels in mouse serum were analyzed through enzyme-linked immunosorbent assay (ELISA) across ages. mRNA levels of APP, APH-1α, PEN-2, and RAGE were determined through polymerase chain reaction (PCR). Thereafter, three degenerative models, including knee osteoarthritis, osteoporosis, and intervertebral disc degeneration, were established. Mice with APP knockout were generated, and the pathology was evaluated at weeks 4-20 through safranin O staining, osteoclast counting (immunohistochemistry, IHC), and hematoxylin and eosin (H&E) staining. Subsequently, TNF-α and HA contents were examined by ELISA, and Col2 expression and apoptosis were also analyzed. Furthermore, the anti-osteoporotic mechanisms of psoralen were explored at the cellular and animal levels.

resultsAs the mice aged, the expression of p-APP increased significantly, while that of proteins involved in the pathway decreased markedly. By constructing an APP knockout mouse model, it was found that after APP knockout, the mice developed bone degenerative lesions, which intensified with age. Intervention with psoralen was effective for ameliorating the pathologic condition of bone degenerative lesions in mice, and inhibiting the progression of bone tissue pathology. Notably, this effect exhibited a dose-dependent trend. Besides, intervention with psoralen in osteoblasts promoted osteoblast proliferation and regulated the phosphorylation of MAPK, AKT, and STAT3. For osteoblasts treated with pathway inhibitors and psoralen, psoralen exerted its effects through the MAPK, AKT, and STAT3 signaling pathways.

conclusionThe phosphorylation of APP promotes the occurrence and progression of bone degenerative diseases. Psoralen regulates bone degenerative diseases by inhibiting APP phosphorylation, and regulating the MAPK and STAT3 signaling pathways.

Indexed as

APP phosphorylationbone degenerative diseasesMAPKPsoralenSTAT3

Identifiers

PMID42491154
PMCPMC13376035

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