ReviewFrontiers in genetics2026
Ferroptosis, lipid metabolism, and genetic regulation in postoperative rehabilitation of elderly hip fractures: from molecular mechanisms to clinical translation.
Review in Frontiers in genetics, 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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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.
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9 authors.
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Abstract
Background: Elderly hip fracture represents a major global public health challenge, with postoperative rehabilitation involving complex molecular mechanisms and metabolic networks. Beyond osteoporotic fractures, pathological hip fractures caused by tumor bone metastasis constitute a non-negligible proportion in elderly patients, with molecular pathological mechanisms significantly different from osteoporotic fractures. Recent research has confirmed that ferroptosis (iron-dependent regulated cell death) and lipid metabolism dysregulation are key links in fracture healing and functional recovery, while genetic polymorphisms, epigenetic modifications, and tumor microenvironment modulate these processes through multiple pathways. Nursing assessment and intervention play an irreplaceable role in promoting functional recovery and preventing complications. Objective: This review systematically elucidates the molecular mechanisms of ferroptosis and lipid metabolism in postoperative rehabilitation of elderly hip fractures (including tumor metastatic pathological fractures), explores the genetic and epigenetic regulatory networks, analyzes multidisciplinary nursing intervention strategies, and provides a theoretical basis for translating basic research into clinical application. Methods: PubMed, Web of Science, Embase, and CNKI were searched to include basic and clinical research published from 2015 to 2025. Keywords included ferroptosis, lipid metabolism, hip fracture, tumor bone metastasis, pathological fracture, genetic regulation, nursing intervention, and muscle atrophy. Results: Ferroptosis participates in secondary injury and inflammatory responses at fracture sites through lipid peroxidation, glutathione depletion, and iron overload. Lipid metabolism dysregulation, especially polyunsaturated fatty acid (PUFA) metabolic abnormalities, not only promotes ferroptosis but also affects bone remodeling and muscle metabolism. Tumor bone metastasis exacerbates ferroptosis after pathological fractures by disrupting local iron metabolism homeostasis, upregulating ACSL4 expression, and promoting oxidative stress. Genetic polymorphisms of key regulatory factors such as GPX4 and FSP1, and DNMT-mediated epigenetic silencing, are closely related to prognosis in elderly patients. Systematic nursing interventions including nutritional management, pain control, early mobilization, and psychological support improve functional outcomes by regulating the oxidative stress-inflammation axis. Conclusion: Ferroptosis, lipid metabolism, genetic regulation, and nursing interventions together constitute a complex regulatory network in postoperative rehabilitation of elderly hip fractures (including pathological fractures), providing multi-level clinical intervention targets. Future research should focus on establishing elderly- and tumor-specific fracture assessment systems, developing highly selective ferroptosis-regulating drugs, advancing clinical translation of multi-omics biomarkers, and building precision multidisciplinary rehabilitation programs integrating nursing care.
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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 Socratic graph.