ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Magnetic Nanoparticles Combined With Pulsed Electromagnetic Field Alleviate Chondrocyte Necroptosis in Osteoarthritis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Impact of pulsed electromagnetic fields on intervertebral disc degeneration: a systematic review of preclinical and clinical evidence.Frontiers in aging · 2026Pooled it
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Chondrocyte necroptosis contributes to the pathogenesis of osteoarthritis (OA). Pulsed electromagnetic field (PEMF) is a potentially useful treatment for OA. Here, magnetic nanoparticles and PEMF generate magneto-mechanical forces for regulating signaling pathways, but their effectiveness remains unclear. This study investigated whether magnetic nanoparticles (MIL-101(Fe)) combined with PEMF alleviate chondrocyte necroptosis in OA. Destabilization of the medial meniscus (DMM) surgery was performed to induce OA in 10-week-old wild-type mice. MIL-101(Fe) and PEMF were applied in human OA chondrocytes and experimental OA mice. Characterization and biocompatibility of MIL-101(Fe) were examined. Chondrocyte necroptosis was analyzed by western blotting, immunofluorescence, TUNEL, and transmission electron microscopy. OA severity was assessed by RT-PCR, immunofluorescence, histology, and micro-CT. We found that MIL-101(Fe) had no obvious cytotoxicity and presented biocompatibility. The combination of MIL-101(Fe) and PEMF ameliorated cartilage metabolism. PEMF attenuated cartilage degeneration and trabecular bone microarchitecture; these protective effects were enhanced by MIL-101(Fe). Further, the combination therapy markedly inhibited chondrocyte necroptosis and significantly decreased phosphorylation of RIP1, RIP3, and MLKL. Together, our findings indicate that MIL-101(Fe) combined with PEMF synergistically ameliorates chondrocyte necroptosis and OA progression without severe side effects, suggesting that this combination therapy may offer a novel strategy for treating OA.
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Registered trials
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