Objects: Traumatic spinal cord injury (TSCI) causes neurological dysfunction below the injured segment of the spinal cord, which significantly impacts the quality of life in affected patients. The phosphoinositide 3kinase/serine-threonine kinase (PI3K/AKT) signaling pathway offers a potential therapeutic target for the inhibition of secondary TSCI. This review summarizes updates concerning the role of the PI3K/AKT pathway in TSCI.Materials and Methods: By searching articles related to the TSCI field and the PI3K/AKT signaling pathway, we summarized the mechanisms of secondary TSCI and the PI3K/AKT signaling pathway; we also discuss current and potential future treatment methods for TSCI based on the PI3K/AKT signaling pathway.Results: Early apoptosis and autophagy after TSCI protect the body against injury; a prolonged inflammatory response leads to the accumulation of pro-inflammatory factors and excessive apoptosis, as well as excessive autophagy in the surrounding normal nerve cells, thus aggravating TSCI in the subacute stage of secondary injury. Initial glial scar formation in the subacute phase is a protective mechanism for TSCI, which limits the spread of damage and inflammation. However, mature scar tissue in the chronic phase hinders axon regeneration and prevents the recovery of nerve function. Activation of PI3K/AKT signaling pathway can inhibit the inflammatory response and apoptosis in the subacute phase after secondary TSCI; inhibiting this pathway in the chronic phase can reduce the formation of glial scar. Conclusion:The PI3K/AKT signaling pathway has an important role in the recovery of spinal cord function after secondary injury. Inducing the activation of PI3K/AKT signaling pathway in the subacute phase of secondary injury and inhibiting this pathway in the chronic phase may be one of the potential strategies for the treatment of TSCI.Xuegang He, Ying Li and Bo Deng contributed equally to this study.

Intervertebral disc degeneration (IDD) is one of the main causes of low back pain (LBP), which severely reduces the quality of life and imposes a heavy financial burden on the families of affected individuals. Current research suggests that IDD is a complex cell-mediated process. Inflammation, oxidative stress, mitochondrial dysfunction, abnormal mechanical load, telomere shortening, DNA damage, and nutrient deprivation contribute to intervertebral disc cell senescence and changes in matrix metabolism, ultimately causing IDD. Natural products are widespread, structurally diverse, afford unique advantages, and exhibit great potential in terms of IDD treatment. In recent years, increasing numbers of natural ingredients have been shown to inhibit the degeneration of nucleus pulposus cells through various modes of action. Here, we review the pharmacological effects of natural products on nucleus pulposus cells and the mechanisms involved. An improved understanding of how natural products target signalling pathways will aid the development of anti-IDD drugs. This review focuses on potential IDD drugs.

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Matricellular proteins are responsible for regulating the microenvironment, the behaviors of surrounding cells, and the homeostasis of tissues. Periostin (POSTN), a non‐structural matricellular protein, can bind to many extracellular matrix proteins through its different domains. POSTN usually presents at low levels in most adult tissues but is highly expressed in pathological sites such as in tumors and inflamed organs. POSTN can bind to diverse integrins to interact with multiple signaling pathways within cells, which is one of its core biological functions. Increasing evidence shows that POSTN can activate the TGF‐β, the PI3K/Akt, the Wnt, the RhoA/ROCK, the NF‐κB, the MAPK and the JAK pathways to promote the occurrence and development of many diseases, especially cancer and inflammatory diseases. Furthermore, POSTN can interact with some pathways in an upstream and downstream relationship, forming complicated crosstalk. This article focuses on the interactions between POSTN and different signaling pathways in diverse diseases, attempting to explain the mechanisms of interaction and provide novel guidelines for the development of targeted therapies.