Peripheral nerve injuries (PNIs) have been mostly reported during the wartimes. The nerve injuries can be caused by gunfire, car crashes, or crushing traumas [1]. The World Health Organization (WHO) stated that car crashes are the leading cause of injury among these and that they also result in a higher number of disabled people. According to reports, the radial and peroneal nerves in the upper and lower limbs are most susceptible to auto accidents [2]. Despite advances in prevention and emergency medical care, morbidity in road accidents is a challenging and growing issue of concern for people all over the world. In most developing nations, the number of injuries and death rates are rising, leading to severe problems. According to WHO statistics, there are 1.5 injuries per second and two deaths every minute. States with the least developed economies account for nearly two-thirds of the victims [3]. The leading cause of mortality among people between the ages of 1 and 34 is trauma [4]. PNI is one of the most common medical conditions in clinics [5]. In America, twenty million people face PNI through medical issues or trauma [6]. Every year, PNI results in neuropathic pain for about 300,000 individuals in Europe, and despite treatment, nerve regeneration is disrupted in almost half of the patients [7].

PNIs are prevalent problems where the nerves are affected, and the extent of damage determines the predominant symptoms. Treatments are inadequate despite a depth of knowledge regarding nerve injury and the regeneration mechanisms [8]. PNIs are severe medical conditions for which there are few options for treatment. One of the most active cases in medical studies up to this point has been PNIs and their treatments [9]. About 3% of all trauma cases encountered in emergency rooms require surgical intervention due to severe PNIs [10].

PNI may result in aberrant axon degeneration, demyelination, or occasionally both. Anytime the myelin sheath is damaged, and the Schwann cells (SCs) are eliminated, demyelination occurs. The nerve conduction velocity is decreased as a result of this demyelination. The axonal integrity of the remaining fibres will allow the conduction velocity to continue normally. Wallerian degeneration (WD) is a crucial biological process based on chemical alterations in the distal nerve following injury. Myelin sheath degradation and axon degeneration occur [11, 12]. The interactions between macrophages and SCs influence the onset of WD. According to research, WD cannot begin until macrophages are drawn into a peripheral nerve that has been injured. Furthermore, macrophages with debris were often found adjacent to intact myelin sheaths, demonstrating that myelin degradation is not only initiated close to degenerated axons. The mechanisms causing myelin disintegration and mitosis, which trigger the secondary responses of SCs, do not take place in WD [13].

Regarding PNIs, various categorizations are occasionally used to describe the fundamental causes of medical loss, such as simple, partly demyelination, or complete axon loss [14]. PNIs are classified into the Seddon and the Sunderland classifications, as shown in Table 1 [15].

After PNI, the functional recovery can be successful thanks to newly sprouting axons. These newly generated axons are able to replace myelin and eventually innervate its motor endplates or sensory receptors [16, 17]. The severity and nature of the nerve injury determine each of these procedures. Proliferation of SC is necessary for the regeneration of axons and nerves. Remyelination and axonal development are crucial for successful nerve regeneration. Regular axonal development occurs at about 1–3 mm/day [18].

Managing PNI continues to be a significant therapeutic challenge. Results were unexpected and depressing following the restoration of the nerves despite advancements in minimally invasive surgical techniques. Understanding the peripheral nerve’s anatomy is necessary to manage various crush injuries. Modern PNI care is predicated on the ability to modify the pathophysiological processes triggered by both injured and healed nerves. Applying a nerve autograft is the best course of action (gold standard) if there is a significant nerve gap. Nerve allografts showed promising results for nerve injuries when nerve autografts are not available [19]. The most recent advancements in peripheral nerve restoration have centered on growth factors and stem cells since nerve grafting remains the gold standard of treatment for severely damaged nerves. The requirements for functional nerve regeneration are intricate. Fibroblast growth factors (FGFs) are released from the ends of injured neurons and are crucial for cell division and regeneration. Studies that combine FGF with structural components have been carried out since then. Additionally, neuronal growth factors (NGF) are vital for the physiological repair and regeneration of the neurons [20].

It is common for the injured peripheral nerve to fail to complete regeneration [21]. Neural regeneration and repair are complex processes that can be affected by multiple factors after PNI [22]. Numerous investigations are still working on immune system modulators, pharmaceutical treatments, and enhancing factors. The therapeutic studies will continue to improve by clinically significant findings from this research [23]. Therefore, the potential positive effects of coenzyme Q10 (CoQ10) on peripheral nerve regeneration following injury are covered in this review.

CoQ10 is present in foods in considerable amounts. Food products such as fish, chicken, nuts, animal meat, and vegetable oils are rich sources of CoQ10 [24]. The different foods have varying amounts of CoQ10 in them [25]. The possible sources of CoQ10 would be via either dietary consumption or endogenous production in the mitochondria [26]. In both plant and animal cells, CoQ10 is a naturally occurring coenzyme. The number of isoprenoids’ side chains can be used to distinguish between each family of coenzymes. Among all coenzymes, CoQ10 is the most popular one that is naturally produced in human mitochondria. The number 10 represents how many times isoprene is repeated. The chemical structure of CoQ10 is 2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone which can be seen in Figure 1 [27, 28].

Animal research has advanced in recent years to uncover contemporary pharmacological therapies [29]. Luckily, in 1957, Dr. Fred Crane discovered the essence of CoQ10 [30]. Over the past 50 years, CoQ10 has played a significant role in transforming mitochondrial bioenergy. Its enzymatic mechanisms facilitate electron transport during adenosine triphosphate (ATP) synthesis. Complexes I and II generally provide electrons [31, 32]. CoQ10 can accept and give electrons through a total of three oxidation pathways. This plays a crucial role in the movement of electrons throughout the mitochondrial membranes to produce ATP energy (Figure 2) [33]. CoQ10 is found in the inner mitochondrial membrane, the site of ATP synthesis. Therefore, the energy required for all essential cellular functions is provided by the ATP that CoQ10 produces [34]. By assisting in the correct reproduction of other antioxidants, CoQ10 promotes cell growth and prevents cell death [35]. It reduces the generation of reactive oxygen species (ROS) in the mitochondria and protects the mitochondrial membrane from oxidative stress [35].

Different body tissues have variable concentrations of CoQ10, which may be related to their metabolic needs. The liver, kidneys, skeletal muscles, and heart have large amounts of it, while the blood plasma contain the least [25]. Oxidative stress and the loss of mitochondrial function may result from CoQ10 depletion inside the mitochondria [33]. Because CoQ10 is essential to all the body’s physiological processes, a decrease in CoQ10 production can harm tissues throughout the body, particularly those that require more energy, such as the kidneys, liver, and heart muscles [25, 36, 37]. The concentration of CoQ10 in plasma is used to determine its levels in humans. A variety of medical conditions can cause tissue deficiencies in CoQ10, such as primary deficiencies in CoQ10, diseases of the mitochondria, dietary deficiencies that impair its synthesis, errors in the formation or utilization of it that are heritable or acquired, and diseases that result in excessive tissue demand [38].

CoQ10 is an antioxidant that can replenish some other antioxidants, like ascorbate and tocopherol. In the human body, it functions similarly to a vitamin. It has a beneficial effect on mitochondrial and neurodegenerative diseases [39]. The presence of CoQ10 in eukaryotic cell membranes raises the idea that it can act as an antioxidant to scavenge free radicals and protect cells from inflammatory processes [40]. One of the fat-soluble molecules, CoQ10, can stimulate cell metabolism and repair cell damage caused by free radicals. The potential benefit of CoQ10 in preventing and treating different clinical diseases associated with oxidative stress has been demonstrated by previous research [41–43]. CoQ10 has been shown in studies to improve peripheral nerve regeneration in patients with diabetic peripheral neuropathy, and the results showed favorable neuroprotective properties in diabetic neuropathy conditions [44]. It can prevent excess fat and improve metabolic abnormalities and insulin resistance brought on by obesity [45]. In histological and immunohistochemical investigations, it was found that CoQ10 reduces interstitial infection, congestion, and cell death [46] and it diminishes interstitial oedema, degeneration of the myofibers, and infiltration of the mast cells [47].

CoQ10 protects lipoproteins from oxidative damage [48], interestingly, it is the only lipid-soluble antioxidant generated endogenously and is regarded as the most crucial lipid antioxidant [28, 49]. Serum or plasma CoQ10 can be utilized to measure intracellular CoQ10 levels, which are influenced by food intake and lipoprotein composition [50]. Research in diverse species has demonstrated the crucial role that CoQ10 plays in cellular energy transfer and its medicinal significance in clinical practice [51]. Overall, the ability of CoQ10 to provide a more active therapeutic level of care to treat certain medical conditions is evident [52].

The great importance of PNI treatment has prompted researchers to look for a suitable antioxidant therapy complementary to curing disorders and injuries affecting the peripheral nerves. Due to its antioxidant properties, CoQ10 has received much research about its utility in managing PNI. Previous articles suggest that, according to the pharmacological and antioxidant properties of CoQ10, it might be a helpful agent for PNI treatment and prevention. Previous studies have mentioned that CoQ10 inhibits apoptosis, lowers oxidative stress, and scavenges free radicals. As a result, it has been found that CoQ10 greatly aided and boosted the myelination of peripheral nerve fibres, promoted the regeneration of peripheral nerves, and improved histological characteristics.