Evidence map›Paper›PMID 41971806›Full record

ArticleFundamental research2026

Harmine ameliorates steroid-induced osteonecrosis of the femoral head by modulating metabolism and ferroptosis via HIF1-α.

Wenming Li, Wei Zhang, Houyi Sun, Wenhao Li, Yi Qin, Liangliang Wang, Jiaxiang Bai, Dechun Geng

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Article in Fundamental 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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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Wenming LiDepartment of Orthopaedics, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Wei ZhangDepartment of Orthopaedics, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Houyi SunDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan 250012, China.
Wenhao LiDepartment of Orthopaedics, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Yi QinDepartment of Orthopaedics, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Liangliang WangDepartment of Orthopaedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Jiaxiang BaiDepartment Department of Orthopedics, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230022, China.
Dechun GengDepartment of Orthopaedics, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Steroid-induced osteonecrosis of the femoral head (SONFH) often leads to disability in the terminal stage, and there are still no effective drugs for prevention. Harmine (Hm), which is extracted from Peganum harmala L., is a β-carboline alkaloid with a number of biological and pharmacological properties. In this study, we discovered the protective effect of Hm on SONFH in rats. In vitro studies showed that Hm could ameliorate oxidative stress and facilitate osteogenic differentiation in bone mesenchymal stem cells (BMSCs), which play an important role in bone development and repair. Bioinformatics analysis revealed that ferroptosis and the HIF1-α pathway played an important role in SONFH pathogenesis. Mechanistically, Hm treatment alleviated ferroptosis by promoting HIF1-α expression in BMSCs. When shHif1a was used to inhibit HIF1-α expression, the protective effects of Hm disappeared. Meanwhile, we further found that Hm intervention promoted HIF1-α expression to increase GSH production and the GSH/GSSG ratio, which further promoted the scavenging of free radicals. In summary, Hm may be a promising candidate for the treatment of SONFH.

Indexed as

AntioxidantsFerroptosisGlutathione anabolismHarmineHIF1-αSONFH

Identifiers

PMID41971806
PMCPMC13069646

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.