Ferroptosis was induced the programmed cell death with iron overload Fenton reaction. Currently, ferroptosis has not been studied thoroughly. Existing studies have confirmed that ferroptosis involves the metabolisms of the Fe, lipids, amino acid, each mechanism is mutually independent but interrelated, and they are formed a complex regulatory network. Other evidence supports that ferroptosis is participated osteoporotic bone remodeling, predominantly affecting the interaction between bone formation and bone resorption, explicitly bone resorption exceeded bone formation. Based on previous studies, this review will summarize the regulatory network mechanism of ferroptosis on bone remodeling and reveal the role of ferroptosis in osteoporosis (OP).

Non-coding RNA (ncRNA) is a type of non-protein-coding RNA molecule transcribed from the genome which performs broad regulation of a variety of biological functions in human cells. The Wnt signaling pathway is highly conserved in multicellular organisms, playing an important role in their growth and development. Increasing evidence suggests that ncRNA can regulate cell biological function, enhance bone metabolism, and maintain normal bone homeostasis by interacting with the Wnt pathway. Studies have also demonstrated that the association of ncRNA with the Wnt pathway may be a potential biomarker for the diagnosis, evaluation of prognosis, and treatment of osteoporosis. The interaction of ncRNA with Wnt also performs an important regulatory role in the occurrence and development of osteoporosis. Targeted therapy of the ncRNA/Wnt axis may ultimately be the preferred choice for the treatment of osteoporosis in the future. The current article reviews the mechanism of the ncRNA/Wnt axis in osteoporosis and reveals the relationship between ncRNA and Wnt, thereby exploring novel molecular targets for the treatment of osteoporosis and providing theoretical scientific guidance for its clinical treatment.

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Inflammation reactions and neuronal apoptosis are the major pathophysiological mechanism of cerebral ischemia/reperfusion injury (CI/RI). Zhongfeng capsules (ZFCs), composed of panax notoginseng, hirudo, red ginseng, eupolyphaga, pangolin scales, rhubarb, and radix salviae miltiorrhizae. It has been reported that composition of ZFCs has a definite curative effect on CI/RI. Thus far, the specific molecular mechanisms of ZFCs remain unclear. This article would set rats model of middle cerebral artery occlusion(MCAO) to research the probable mechanisms of ZFCs underlying inflammation reactions and neuronal apoptosis signaling pathways. Our analyses revealed that in the ZFCs treatment group, there was an obvious decrease in neurologic impairment, as well as alleviation of the area of cerebral infarction, cerebral edema, histopathologyrats and neuronal apoptosis were also alleviated. The IL-1β, IL-6, and TNF-α were found to be down-regulated expression in the ZFC treatment group as well as the expression of Bcl-2, p-PI3K, p-Akt, and I-κBα was increased and the expression level of TLR4, NF-κB, Bax, caspase-3 was tended to decrease. The results indicated that ZFCs was effective in protecting the brain against CI/RI. One of their neuro-protective mechanisms may be associated with TLR4/NF-κB signalling, and they may negatively regulate the transcriptional activity of NF-κB and the secretion of downstream inflammatory factors. Another of their neuro-protective mechanisms may occur by regulating the expression of Bcl-2-Bax proteins of PI3K/Akt pathway. Our findings could facilitate that the suppressing PI3K/Akt signal pathway-mediated neuronal apoptosis, suppressing TLR4/NF-κB signal pathway-mediated inflammatory reaction were the potential mechanisms for the regulations, activation of PI3K/Akt pathway can inhibit the secretion of proinflammatory cytokines, which may be another functional mechanism of ZFCs against CI/RI.

Osteoporosis (OP) is characterized by a decrease in osteoblasts and an increase in adipocytes in the bone marrow compartment, alongside abnormal bone/fat differentiation, which ultimately results in imbalanced bone homeostasis. Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteoblasts and adipocytes to maintain bone homeostasis. Several studies have shown that lncRNAs are competitive endogenous RNAs that form a lncRNA–miRNA network by targeting miRNA for the regulation of bone/fat differentiation in BMSCs; this mechanism is closely related to the corresponding treatment of OP and is important in the development of novel OP-targeted therapies. However, by reviewing the current literature, it became clear that there are limited summaries discussing the effects of the lncRNA–miRNA network on osteogenic/adipogenic differentiation in BMSCs. Therefore, this article provides a review of the current literature to explore the impact of the lncRNA–miRNA network on the osteogenic/adipogenic differentiation of BMSCs, with the aim of providing a new theoretical basis for the treatment of OP.