Growth factors, which are cytokines with activity of stimulating cell growth, are composed of polypeptides and protein and are used to regulate cell growth and other cell functions. They are found in platelets, various adult and embryonic tissues, and most cultured cells (Burnouf et al., 2013). It can directly reach the nucleus to repair genes and promote cell division, reproduction and regeneration (Escobar et al., 2015). The general characteristic of GF biological preparations is that it can bind to cell membrane specific receptors and modulate the growth and development of cells. At present, Fibroblast growth factor (FGF), bone morphogenetic protein (BMP), nerve growth factor (NGF), granulocyte colony stimulating factor (G-CSF), platelet-derived growth factor (PDGF), transforming growth factor -α and transforming growth factor -β are all GF related to sports injury. Sports injuries are generally caused by professional sports and recreational sports injuries. Muscle injury usually occurs after eccentric contraction, resulting in injury of tendon joint. When the degree of injury is different, the doctor’s treatment method will also change. But mainly limited to ice compress, oppression, elevation, anti-inflammatory drugs, rest, and activities (Kasemkijwattana et al., 2000). Motor injury generally exists in muscle tissue, bone and other parts of the human body. The spontaneous regeneration ability of muscle tissues and bones is poor, and usually they cannot be fully recovered after injury (Lyu et al., 2020). Once the muscle and bone are damaged, due to the formation of adhesion and scar, the normal biological and biomechanical properties of tendon and bone cannot be completely regained (Giannotti et al., 2015). These abnormal arrangements and structures are often the risk factors for re-injury. Sports-related injuries include acute and chronic injuries. For soft tissues including muscles and ligaments, no matter what kind of injury is, it includes four processes: hemostasis, inflammation, proliferation of cells and matrix, wound maturation and remodeling. The difference lies in the time limit. In the above-mentioned processes, the cell and matrix proliferation stage can be said to be the most important stage of wound healing, determining whether the function of soft tissues is likely to return to the previous level. In addition, the stages of wound maturation and remodeling may involve the formation of scar tissue. Moreover, physiopathologic and metabolic factors in the body can affect any process of injury repair, resulting in prolonged time. In the process of potentially unfavorable repair, it leads to the instability of the soft tissue structure and the weakening of its function, resulting in re-injury. (Middleton et al., 2012)Movement-related GF can affect the cycle conversion of target cells to accelerate the division and proliferation of cells (Creaney and Hamilton, 2008), and promote the synthesis of DNA, RNA and protein in tissue repair cells, which can effectively eliminate low density lipoprotein in blood (Evanson et al., 2014). It plays a significant regulatory part in wound inflammation and infection, wound healing, differentiation of various cells (Gigante et al., 2013), and apoptosis of aging cells in the human body (Bachl et al., 2009).

GF formulations have described a number of fascinating results in sports medicine (Bisciotti et al., 2013), however, the biological characteristics of many different GF preparations are not well understood. A variety of GF preparations can be used in combination, which makes the effect better in the repair of sports injury. However, the effect of using GF preparation in the treatment of motor injury may also be poor, so we must pay attention to the implementation of the course of treatment and the role of the site. In this paper, the source, properties, action mechanism and possible effects of GF preparations in the field of sports injury were introduced in detail. The course results of future GF preparations for the treatment of sport injury were also summarized in order to promote the development of GF preparation therapy.

Bone morphogenetic protein-2 and PDGF are the barrier membranes of osteogenic growth factors, and they have studied the loading and release kinetics of growth factors more through soaking in GF solution and culturing the membrane followed by freeze-drying, or mixing with polymer before evaporation to incorporate GF into the membrane (Zumstein et al., 2011). Membrane materials and other reagents are important factors that affect the adsorption capacity of the membrane, as well as the concentration of heparin, crosslinking agent and GF. Notably, there were two stages of release of GF from the membrane: the first stage consisted of a sudden release (approximately 1 day) and the second stage consisted of a slow release. In addition, the ability to exert biological activity at GFs concentrations controlled by release in the membrane has also been demonstrated by many studies. For example, white blood cell and platelet-rich fibrin (L-PRF) contains growth factors. L-PRF clots were slowly released with increasing GF1, PDGF-AB over the first 8 h, and within the first 7 days increased complete release of growth factors GF1, VEGF, and MPO and then decreased to near zero at Day 28.

Studies have shown that there are several methods for delivering higher doses of GF to injured tissues, but most rely on platelet release of GF. The alpha particles of platelets contain GF [insulin-like GF-1, vascular endothelial GF, and transformed GF-β (1)],etc. Platelet-rich plasma is usually analyzed for peripheral blood using different types of centrifugation, and different separation methods result in different distributions of platelet and leukocyte counts (Pochini et al., 2016). A standard L-PRF centrifugation protocol at 400 ×g has been shown to have the highest concentrations of platelets and leukocytes (Zumstein et al., 2012).

Plasma (PRGF) therapy, direct injection and hydrogel incorporation can be realized at the injury site as can be seen in Figure 1. 1) Plasma treatment refers to the reinfusion of plasma in the body. After removing red and white blood cell, platelets, and liquid components from that blood, the remaining material contain large amounts of growth factors, coagulation factors, albumin, globulin, and various antibodies. 2) Direct injection, which can be used as a liquid injection preparation for damaging tendons or joints (Singh et al., 2020). Pure platelet-rich fibrin (P-PRF) and leukocyte and platelet-rich fibrin (L-PRF) are leukocyte-free and leukocyte-containing solid fibrin-based products, respectively, that can be used as bioactive healing biomaterials (Creaney et al., 2011). 3) Hydrogel therapy. Treatment of motor injury requires consistent skeletal muscle regeneration, complete healing as far as possible, and reduction of tissue fibrosis (Hwang et al., 2013). It has been studied that stem cells and basic fibroblast growth factor (BFGF) are incorporated into hydrogels to observe muscle cell regeneration in animal models of muscle tearing (Caballé-Serrano et al., 2019). The results showed that the rapid twitch muscle contraction at the injury site was markedly improved, and fibrosis was markedly reduced. Combined treatment with GF hydrogel results in restoration of function, revascularization and innervation with minimal fibrosis of the torn muscle. Thus, some of the GF hydrogel preparations could be used as a hopeful treatment for muscle cells’ regeneration, and this part of the study needs to be further developed.

In terms of the effect of activator on promoting the use of GF, some studies have found that the activator used in combination with PRP is effective for promoting the concentration of GF. Such as the effect of activator calcium chloride on the concentration of GF, activated and inactive calcium chloride prepared by PRP under each condition, activated with calcium chloride resulted in significant increases in PDGF antibody and IGF-1 concentrations, and calcium chloride activated PRP resulted in the release of platelet-differentiated GF (Hamilton et al., 2015). The use of these activators affects the outcome after treatment of motor injury and is recommended for consideration in future treatment.

GF is the key to regulate cell signaling pathway. Currently, the inhibition of GF is exerted through signal transduction inhibitors. It can interfere with the process of protein-protein interaction between GF and its receptor by targeting the extracellular protein-binding domain of GF receptor. Such as the signal transduction inhibitor compound CJJ300, inhibits tgf-beta signals by disrupting the process of formation of signal complexes that transform gf-beta (tgf-beta) (Wu et al., 2020). The compounds can be used for treating the elimination of downstream signals during the transmission of cell signaling pathways, the phosphorylation of GF in key factors of the pathways and the induction of molecular markers. Through these effects, signaling inhibitors can significantly inhibit cell migration.

In addition, there is a method for producing an inhibitory effect on GF by inhibition of a transcription factor. Mechanical GF (MGF) can significantly promote the migration of chondrocytes from growth plates, accompanied by YAP activation. YAP is a transcription regulator that modulate cell proliferation, survival, and differentiation, in order to control organ development and tissue regeneration (Jing et al., 2018). Knocking out YAP with the YAP inhibitor YAP siRNA inhibits MGF-induced migration. MGF promotes YAP activation through RhoA GTPase-mediated cytoskeletal recombination, and C3 toxin can also be used to inhibit RhoA and eliminate MGF-induced YAP activation.

With the development of GF biological agents, many studies began to study GF inhibitors to achieve the purpose of inhibiting GF and controlling its action mechanism.

Muscle damage is a common cause of long-term severe pain and limb disability. Recovery from muscle damage caused directly or indirectly by exercise is a complex but well-defined process that includes degeneration, inflammation, regeneration, and fibrosis. Biological agents, such as IGF-1, MGF, PDGF, and TGF-β have been discussed in clinical treatment. They have the potential not only to treat athletic injuries but also to be a centre of interest for stimulant abusers as biotechnologies that achieve good athletic performance but are not yet fully understood.

The research have shown that: 1) GF biological agent therapy is a very promising treatment for motor injury, which is based on the power of autologous growth factor (GFs) to accelerate tissue healing, promote muscle regeneration, increase angiogenesis, reduce fibrosis, and make the muscle injury rapid recovery. 2) There are various methods for delivering the higher dose of GF to the injured tissue, but most of them depend on the platelet release of GF. At the site of injury, there are several ways to deliver higher doses of GF to the injured tissue. 3) At present, the inhibition of GF is mainly through signal transduction inhibitors and inhibition of transcription factor production. 4) Pattern of GF during wound repair: GF directly regulates many key steps of normal wound repair, including inflammatory cell chemotaxis, division and proliferation of fibroblasts, keratinocytes and vascular endothelial cells, formation of new blood vessels, and synthesis and degradation of intercellular substances. 5) When GF promotes chronic wound healing, in most cases, certain GF can be used targeted only when in vivo regulation still cannot meet the need for repair.

To date, most treatments for muscle injury with GF biologics have been due to limited experimental and clinical data or only empirical trials. Therefore, we need more experimental studies, including the specific GFs to quantify the release of PRP, angiogenesis, myogenesis and functional recovery data, as well as other mechanisms of GF repair, to finally verify the repair hypothesis of GF biological agents in the treatment of muscle injury and open a new journey for its wide clinical application. Currently, there is a large amount of data on the pathophysiology of muscle injury in the relevant studies.