Adipose tissue contains a heterogeneous population of cells, which only consist of approximately 20% lipid-rich adipocytes [19]. The rest of the cell population comprises stem cells, neural and vascular progenitor cells, multipotent progenitor cells, pericytes, fibroblasts and endothelial cells, eosinophils, macrophages, and innate lymphoid cells (ILCs), T cells, and B cells [7, 19]. Adipose tissues also contain adipokines, including leptin and adiponectin, which can be considered as stem cell inducers [19, 20].

There are two main types of adipose tissue, which differ in function—white (WAT) and brown (BAT) adipose tissue. WAT is responsible for the main energy storage in the organism, while BAT is an energy expenditure and protective tissue [7, 20]. Moreover, it has been shown that adipocytes from WAT can undergo differentiation in adaptive responses and reversible change functions that make them similar to BAT cells (beige AT), thereby demonstrating the plasticity of adipose tissue [20]. WAT is localized subcutaneously, intra-abdominally, epicardially, and gonadally, while BAT is interscapular, paravertebral, perirenal, cervical, and supraclavicular [21]. However, due to the ease and non-invasive harvesting procedure by liposuction, subcutaneous AT is most widely considered as a source of adipose-derived mesenchymal stem cells rather than its other localizations in the human body [7]. Importantly, uncultured stromal vascular fractions (SVFs) from adipose tissues can usually obtain up to 3% of the ASCs. However, it has been shown that SVFs from subcutaneous liposuction aspirates can contain even 10% of the ASCs [19, 22].

In clinical use, the type of adipose tissue, its harvesting area, tissue origin, age, weight, disease state, race and ethnicity, and body mass index of the donor are important factors in providing high-quality ASCs [7, 22]. It has previously been shown that ASC proliferation, differentiation potential, and growth factor secretion from older donors are lower [23, 24, 25, 26]. Moreover, the more the patient weighs may also affect lower self-renewal and angiogenic capacity but can also provide a higher adipogenic potential in isolated ASCs [7, 27, 28]. It has been also shown that smoking, diabetes mellitus, hypercholesterolemia, and hypertension have negative effects on the regenerative potential of ASCs [27, 29].

Bone marrow is a source tissue from which mesenchymal stem cells are isolated, as defined for the first time by Friedenstein et al. [6]. Although it is commonly used for research in regenerative medicine, BM as a source of MSCs also has its limitations. Obtaining tissue to isolate MSCs is an invasive procedure that can cause the patient pain and infection [24, 30].

Bone marrow, as a site for hematopoiesis, contains hematopoietic (blood cells lineages committed progenitors, stem cells) and non-hematopoietic cells (nervous system cells, adipocytes, fibroblasts, osteoblasts, osteocytes, osteoblastic precursors, mesenchymal stem cells) [6, 31]. There are two types of BM that differ in function—red (where hematopoiesis occurs) and yellow (fat storage) [32].

It is worth noting that bone marrow is a less effective source of MSCs than adipose tissue. While MSCs form 3% of adipose tissue, their content is even lower in BM (0.002%) [19]. Moreover, BM-MSCs are characterized by faster senescence and lower proliferation capacities than ASCs during expansion, and it is very important to provide medical products of high quality as fast as possible to treat the patient [1]. Adipose tissue is also a better candidate for use in regenerative medicine due to its similar properties for differentiation as BM-MSCs, yet has an easier obtaining procedure and culture expansion. However, some studies have reported better osteogenic potential in BM-MSCs than ASCs, although those studies were performed on MSCs acquired from different donors. Additionally, the MSC origin may be crucial and adaptation of the source tissue for medical purposes may depend on the disease [1, 24].

Many studies have shown that appropriate EMF stimulation affects the proliferative potential and cell cycle of MSCs; however, various different effects have been observed, which suggests that the effects are dependent on the EMF parameters and stimulation times [12, 13, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47].

A frequency of 50 Hz is a recognized parameter of electromagnetic fields emitted by everyday devices and has aroused the interest of researchers [34]. Li et al. [35] showed that pulsed electromagnetic fields (PEMF) (50 Hz; 10 mT) stimulation can increase the proliferation of rat MSCs after 3 and 6 h of exposure but also influence the cell cycle by increasing the percentage of cells in the G1 phase. Importantly, in that study, EMF exposure did not influence stem cell viability. Results by Li et al. [35] were a one-time effect, since, after 16 h of EMF exposure, no effect was again observed on MSC proliferation and cell cycle. In other studies, MSCs were repeatedly exposed to EMFs during the culture time with different outcomes. Fan et al. [36] and Seo et al. [37] showed that MSC proliferation increased after EMF exposure (50 Hz; 1 mT). Conversely, in work conducted by Seo et al. [37], the observed changes in proliferation were not statistically significant. Interestingly, Fan et al. [36] showed smaller changes in G2-phase cell percentage, contrary to Li et al. [35]. However, in both works, the authors indicated changes in the percentage of MSCs in S-phase post-exposure; nevertheless, as noted by Li et al. [35], this effect appeared detectable and significant 1-hour post-EMF exposure but not after 16 h [36]. This observation suggests that MSCs undergo adaptive responses to environmental conditions, such as EMFs, thereby indicating that stem cell fate can be modulated.

Alongside the 50 Hz frequency, scientists have also often studied the effects of EMFs with a frequency of 15 Hz. The results published in various research papers showed that 15 Hz can increase proliferation. Data published by Jazayeri et al. [38] showed that proliferation, after EMF exposure (15 Hz; 0.2 mT), increased, and the longer the culture underwent EMF stimulation the higher the effect. It has been shown that seeding density does not influence proliferation changes by EMF (15 Hz) stimulation; however, Sun et al. [39] showed that the slight observed increase reflected the entry of more bone marrow MSCs into the G2/M-phase at the beginning of the experiment. The number of cells at the G2/M-phase increased at the beginning and decreased after 18 h along with the number of MSCs in the S-phase, although S-phase was not affected at the beginning. Sun et al. [39] also showed that after 18 and 24 h of EMF exposure, a statistically significant higher percentage of MSCs entered into G0/G1-phase, although this effect was not observed after 30 h of EMF exposure. Song et al. [40] also discovered that the proliferation of MSCs after EMF stimulation (15 Hz; 1 mT) increased significantly after 7 and 10 days, however, this effect did not last until day 14. Similarly, using the same EMF parameters (15 Hz; 1.5 mT), other studies have also shown increased proliferation after 7 days of EMF stimulation [12, 41, 42].

Other frequencies of EMF than 15 Hz and 50 Hz were also studied. Ross et al. [43] showed a slight increase in BM-MSC proliferation using EMFs (5 Hz; 0.4 mT) for 10 min per day. However, an improved biological effect was achieved by Bloise et al. [44] (75 Hz; 2 mT, 20 min/day). A slight increase in proliferation was also shown by Poh et al. [45] (26 Hz). Thus, several studies showed EMF can increase MSC proliferation, yet Zhang et al. [13] showed no significant changes in proliferation after EMF stimulation (7.5, 15, 30, 50, 75 Hz; 1 mT) alongside results presented by Parate et al. [46] (15 Hz; 2 mT). Moreover, Yan et al. [47] indicated that EMF treatment (50 Hz; 20 mT) can inhibit MSC proliferation. The different studies on the effects of the influence of EMFs on MSC proliferation are presented in Table 1 (Ref. [12, 13, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48]).

The mechanisms involved in EMFs (with different parameters) influencing MSCs remain unclear owing to a lack of exploration. However, it is known that the MEK/ERK signaling pathway is involved in cell proliferation, while it has been shown that EMFs (15 Hz; 1 mT) stimulate proliferation through this pathway [40]. Similarly, EMFs (26 Hz) can increase the number of phosphorylated ERK 1/2 proteins suggesting that EMFs activate the MEK/ERK pathway in MSCs [45]. EMFs can induce cellular stress and promote increased reactive oxygen species (ROS) generation, which can become free radical ions. ROS are highly reactive signaling factors that are naturally produced by cells, and depending on concentration may have different effects on cells, including inhibiting proliferation [11]. Moreover, ion influx changes (K${}^{+}$ and Ca${}^{2+}$ affect activated potassium channels) after EMF treatment may affect G1- to S-phase cell cycle progression in undifferentiated MSCs, thereby promoting proliferation (cell control proliferation process mostly occurs at phase G1) [38, 39, 49]. These determinations correlate with the requirement of prolonged ERK 1/2 activation for cyclin D1 transcription, which promotes cells from G1- to S-phase [40, 49]. As shown by Marędziak et al. [50], static magnetic fields (sMFs, 0 Hz; 0.5 mT) can also promote the proliferation of MSCs via the PI3K/Akt pathway. Similarly, Poh et al. [45] and Ferroni et al. [51] showed that activation of the Akt signaling cascade in MSCs after EMF exposure (26 Hz), alongside ERK 1/2 activation, can promote proliferation. Importantly, extrinsic factors, such as EMFs, can potentially influence symmetric and asymmetric stem cell divisions via the targeting of tubulin dipoles in the spindle microtubules during cell division [11, 52]. Interestingly, it has been also shown that EMF (50 Hz; 1 mT) can increase the proliferation of human periodontal ligament mesenchymal stem cells (PDLSCs) in vitro [48].

Overall, EMFs can have different effects on the proliferation of MSCs depending on the parameters and duration of stimulation. EMFs have the capacity to enhance proliferation but only at specific parameters, which can be a useful tool in stem cell-based therapy, to accelerate the regeneration process via an increased number of cells capable of differentiation as well as cytokine and growth factor secretions.

MSCs offer great potential for use in regenerative medicine because of their unique secretome. In particular, ASCs deserve special attention here in relation to cell therapy owing to the extensive number of factors that they secrete, especially cell-free therapy. ASCs secrete cytokines, proteins, growth factors, and non-coding RNAs, which are carried by exosomes, and all offer great therapeutic potential. Most importantly, it was shown that EMFs with appropriate parameters can modulate the secretion of these compounds [7, 53].

EMFs can enhance regenerative properties by modulating specific signaling pathways, gene expression, and protein secretion (Table 2, Ref. [17, 36, 44, 46, 54, 55, 56, 57, 58]). Immunomodulatory properties can be also mediated by EMFs [36, 46, 54]. Fan et al. [36] showed increased expression of cytokines, such as IL-11, IL-7, LIF, SCF, M-CSF, and TPO by BM-MSCs after EMF (50 Hz; 1 mT) stimulation but no influence in IL-6, IFN-$\gamma$, and TNF-$\alpha$ was observed. In contrast, it was also shown that EMF (5.1 Hz; 0.4 mT) can reduce the secretion of proinflammatory cytokine IL-6 as well as other proinflammatory molecules, such as IL-1b, IL-17A, and TNF-$\alpha$. Ross et al. [54] also showed that EMF stimulation may stabilize the secretion of anti-inflammatory cytokines (IL-3, IL-4, and IL-10). However, Parate et al. [46] showed that EMF stimulation can significantly increase IL-10 secretion as well as BMP-2, BMP-4, TSP-2, and IL-1Ra by MSCs in non-differential medium after EMF exposure (15 Hz; 3 mT). Importantly, conditioned medium (CM) after EMF stimulation showed properties to reduce inflammation and the cellular apoptosis of chondrocytes and naive MSCs [46].

EMFs can also modulate the trophic activity of MSCs. It has been shown that EMFs increase the secretion of IGF-2 [46], VEGF [17, 46, 50, 55, 56], FGF-2, and PDGF [17], although the efficiency was dependent on the EMF parameters being applied. Studies also have shown that EMFs can influence TGF and BMP protein secretion, which is linked to the capacity of EMFs to enhance MSC differentiation [46, 57, 58]. EMFs (75 Hz; 2 mT) have been shown to slightly increase the deposition of osteogenic proteins (ALP, COL, FN, OPN, OSC, and OSN) in the cell matrix in a proliferative medium [44]. EMFs can also impact BDNF and NGF secretion [17, 55]. Huang et al. [55] showed that treating BM-MSCs with PEMFs (50 Hz, 1 mT) significantly increased BDNF and VEGF expression in vitro via the Wnt/$\beta$-catenin pathway. Moreover, they proved that the use of BM-MSCs and EMF stimulation increased BDNF, NGF, and VEGF expressions in vivo alongside enhancing neuron preservation and increasing axonal growth in mice with spinal cord injuries. It is important to note that the MSC secretome is often enclosed in microvesicles, which encapsulate target molecules as a specific drug system delivery [58]. However, in the literature, to the knowledge of the authors of this manuscript, there is a lack of studies on the influences of EMFs on human MSCs exosome secretion and their cargo. Moreover, there is still a small number of studies showing the effect of EMFs on the biology of ASCs, while they are great candidates for stem cell-free therapy [7].

The ability to enhance the anti-inflammatory properties of MSCs may represent an important new approach for the treatment of autoimmune diseases. Moreover, modulating the concentrations of cellular trophic factors may provide a crucial improvement in cell and tissue regeneration. However, as described and summarized in Table 2, the effects may vary depending on the EMF parameters and exposure time.

Mitochondria are extremely important organelles since they undertake the main processes of energy metabolism and adenosine triphosphate (ATP) production. These organelles also control various processes, such as cell signaling, ROS production, as well as calcium ion flow and concentration, thereby playing an important role in the proper course of key biological functions, such as differentiation or apoptosis. In response to internal and external signals, mitochondria initiate dynamic processes, such as mitochondrial fusion and fission, increasing mtDNA copy and respiratory enzymes level, enhancing oxygen consumption rate (OCR), and intracellular ATP levels to meet the metabolic demands of the cell [59, 60].

According to existing data, changes occurring under the influence of EMFs suggest that MSCs are vulnerable to this biophysical factor and try to adapt to new environmental conditions by changing their metabolism. MSCs are characterized by low mitochondrial activity and glycolytic state due to their dormant form in stem cell niches unless cells undergo differentiation (changing their fate), which requires a high energy demand [9, 60, 61]. Hollenberg et al. [9] showed that EMFs (10 Gauss for 4 days) significantly increased mitochondrial membrane potential in BM-MSCs indicating increased oxidative phosphorylation (OxPhos), and thus, mitochondrial activity and ATP production. Furthermore, a study conducted by Ehnert et al. [62] showed that EMFs (16 Hz and 26 Hz) can significantly increase mitochondrial activity in an osteoblast and ASC co-culture after 7 and 14 days (5 times per week for 7 min each day). Interestingly, Celik et al. [63] showed that the X-directed application of PEMFs (1 mT) has a greater effect on mitochondrial respiration than Z-directed stimulation. EMFs can influence the influx of ions, and thus, the mitochondrial membrane potential [9, 33]. Since mitochondria store Ca${}^{2+}$ and EMF can modulate calcium ion influx and disrupt Ca${}^{2+}$ homeostasis, electromagnetic fields are likely to affect mitochondrial activity through calcium ion oscillations. Then, mitochondrial activation can lead to further changes in MSCs and new stem cell fate decisions [33, 44]. It is also worth noting that ASCs, similar to BM-MSCs, use a mixed metabolism that is based mainly on glycolysis and mitochondrial activity, which is reflected in the secretion of lactate and citrate. However, it has been shown that even ASCs isolated from the same type of adipose tissue, i.e., white adipose tissue, may differ in metabolism, which indicates the heterogeneity of this tissue. Lefevre et al. [64] demonstrated that mesenchymal stem cells from visceral adipose tissue (V-ASC) secrete higher concentrations of lactate than those isolated from subcutaneous adipose tissue (S-ASC), indicating their greater preference for glycolysis. Moreover, they showed that S-ASCs in cell culture without glutamine limit the pyruvate pathway towards lactate synthesis, yet the same does not occur in the V-ASCs. These differences should be considered in further studies on the effects of EMFs on ASC metabolism.

EMFs can both influence mitochondrial activity by switching glycolysis to OxPhos and increase mitochondrial DNA (mtDNA) copy numbers. Bai et al. [65]showed that EMF (50 Hz; 5 mT) increased the mtDNA copy number of BM-MSCs in a time-dependent manner, which may suggest that cells prepare for an increase in mitochondrial activity and higher cell energy demand needed for stem cell differentiation or division. It is worth mentioning that EMFs might influence mitochondrial migration, and the results we obtained showed that cells stimulated with EMFs (50 Hz; 1.5 mT) had mitochondria located closer to the periphery of the cell [data in press]. This finding may be important in understanding the regenerative potential of EMF-stimulated MSCs via mitochondrial transfer to other cells [60] since there are not many studies investigating mitochondrial transfer in physiological conditions [66].

Studies have shown that EMFs can influence mitochondria functioning; however, the clear mechanism of action remains unknown (Table 3, Ref. [9, 62, 63, 65]). It is suggested that EMFs induce mitochondrial ROS production on a non-toxic level (activating TRPC1-mediated calcium entry) as well as interfere in Ca${}^{2+}$ homeostasis in the mitochondria, which in turn may activate pathways responsible for mtDNA replication, OxPhos activation, and stem cell differentiation [33, 62, 63, 65].

Electromagnetic fields can affect the ion influx of MSCs by inducing the vibration of free ions and disturbing the electrochemical potential on the cell membrane surface. This process may in turn affect the transmembrane receptors, phospholipids, and in effect specific pathways that modulate stem cell proliferation, differentiation, viability, metabolism, apoptosis, cell–cell communication, and signaling with extracellular matrix components that influence the stem cell fate [33, 67]. Below, we present studies (Table 4, Ref. [13, 44, 47, 68, 69, 70, 71]) and briefly describe the influence of EMFs on K${}^{+}$, Na${}^{+}$, and Ca${}^{2+}$ channels and ions influx only in MSCs. However, most studies have focused on the examination of calcium channels and Ca${}^{2+}$ flow after EMF exposure. Moreover, to the knowledge of the authors, no studies have been performed on the effects of EMFs on the flow of ions in ASCs.

Yan et al. [47] showed increased K${}^{+}$ and Na${}^{+}$ ion concentrations in BM-MSC culture supernatants after EMF exposure (50 Hz; 20 mT). Moreover, it has been shown on different cell lines that LF-EMFs affect the K${}^{+}$ current flow through the cell membrane by affecting the A-type K${}^{+}$, delayed rectifier K${}^{+}$, M-type K${}^{+}$, fast-inactivating transient (IK, A), and dominant-sustained (IK, V) potassium channels [33]. It is also suggested that calcium-activated potassium channels have a significant influence on the differentiation of MSCs via intracellular calcium oscillation and membrane potential [72].

EMFs can also increase calcium currents [72] and the intracellular concentration of calcium ions in MSCs [13, 44, 47, 68] by activating the L-type voltage-gated calcium channels (VGCCs) through membrane depolarization [68, 69] and significantly increasing the expression of VGCC-related genes (CACNA1E and CACNA1G) [67, 69]. Interestingly, two independent studies showed that EMF exposure at different parameters did not influence CACNA1C gene expression related to the VGCC [69, 70]. Moreover, it has been shown that EMFs increased the expression of the TRPC1 and TRPV4 genes involved in the entry of calcium through the cell membrane [70] as well as P2X7 purinergic receptors related to the transport of sodium, calcium, and potassium [71]. Influencing calcium channels may have an effect on the differentiation and migration of MSCs, while Zhang et al. [13] showed that EMF-mediated changes in Ca${}^{2+}$ concentration activated the Focal Adhesion Kinase/Ras homologous Guanosine Triphosphatase (FAK/Rho GTPased) migratory signaling pathway [33]. The importance of Ca${}^{2+}$ influx may be due to its possible modulation of calpains, which are involved in post-translational protein regulation, as well as epigenetic regulation via DNA and histone modifications [73].

Electromagnetic fields can influence ion influx, and thus, regulate stem cell functioning, which may be useful in the context of using MSCs as therapeutic treatments. Calcium has the potential to regulate stem cell fate mediated by EMF, while the disturbance of this concentration may lead to both desired and undesirable effects, such as faster differentiation, increased proliferation, or cell death. More research is needed on the effects of EMFs to explore the impact of EMFs on the flow of ions in MSCs, especially from sources other than BM-MSCs.

Many in vitro and in vivo studies have demonstrated that electromagnetic fields can also influence the differentiation of mesenchymal stem cells [9, 10, 12, 33]. EMFs influence the influx of ions, and thus, the concentration across the cell membrane and transmembrane potential. In turn, this influences cell–cell communication and cell physiological processes, thereby modulating stem cell fate by triggering epigenetic changes and gene expression towards the activation of differentiation pathways [10, 11, 33, 74]. Electromagnetic fields, as suggested by Bai et al. [65], may cause the MSCs to become more sensitive to environmental changes, which leads to easier differentiation. In fact, EMFs influence Ca${}^{2+}$ influx. Calcium is a known cyclic AMP activator—a crucial component that triggers metabolic processes [10]—indeed, studies have already demonstrated that during differentiation, the demand for energy increases, which causes the mitochondria to alter [9, 62, 63, 65]. Moreover, the induction of ROS, which are reactive signaling factors, through EMF stimulation, can affect ATP production and activate differentiation pathways [9, 10, 11]. Easier differentiation of MSCs after EMF stimulation may also be affected by its influence on spindle microtubules (due to tubulin dipoles), thereby leading to asymmetrical cell divisions [11, 74]. However, knowledge is still limited regarding the influence of EMFs on symmetric and asymmetric stem cell divisions. In this review paper, we do not extensively discuss the effect of EMFs and the mechanisms involved in MSC differentiation. There are many up-to-date and well-written papers that only focus on this topic already published [9, 10, 12, 33].

Clinically, most interest is focused on the chondrogenesis and osteogenesis of MSCs, while neurogenesis has also been widely studied. Previously, Safavi et al. [10] published a systematic review covering the topic of MSC differentiation based on literature published up to December 2021. In this review paper, we only collected research papers available in PubMed that studied MSC chondrogenic, osteogenic, and neural differentiations published between January 2022 and July 2023 (Table 5, Ref. [48, 55, 56, 75, 76, 77, 78, 79, 80, 81]).

Recently, Huang et al. [55] showed that a combined treatment of EMF (50 Hz; 1 mT) and BM-MSCs may enhance and promote spinal cord injury treatment in a mice model by increasing the expression of NGF, BDNF, and VEGF. It has been also reported that EMFs can increase neuron preservation (NeuN and NF-200) and increase axonal growth (MBP, myelin sheath) [55]. Moreover, it has been shown that an approach combining EMFs and MSCs may be successful for use in cerebral ischemic models. Park et al. [75] showed that EMFs (60 and 75 Hz; 10 mT) can increase the protein expression of MAP-2 and NF-L in cell cultures of BM-MSCs, while BM-MSCs/EMF (60 Hz; 10 mT) treatment can reduce inflammation and significantly improve behavior and motor coordination in a cerebral ischemic mice model after treating for 13 days. Interestingly, Guo et al. [82] managed to provoke ASCs to undergo neuronal differentiation by using biodegradable graphene film, which acted like a wireless electrical signal generator led by electromagnetic induction.

Seonwoo et al. [76] studied the effects of applying reduced graphene oxide-incorporated natural calcium phosphate cements (RGO-CPCs) and EMF (50 Hz; 0.6 $\pm$ 0.05 mT) to improve the osteogenic differentiation of MSCs and found that this approach was not severely toxic and could enhance the differentiation process. Recently, research by Gerdesmeyer et al. [56] showed that EMF (3 Hz; 80 mT, 150 mT) stimulation can increase the expression of markers related to osteogenesis and chondrogenesis, although the effect was not statistically significant. Additionally, Ren et al. [77] showed that BM-MSCs cultured on Fe${}_3$O${}_4$-TNrs (titanium dioxide nanorods) presented with better pro-osteogenic properties after EMF treatment (15 Hz, 1 mT), showing higher expressions of osteogenic markers, such as ALP, OCN, RUNX2, and OPN. Moreover, this biomaterial improved osseointegration femur defects in a rat model after EMF stimulation in vivo [77]. Interestingly, EMFs (50 Hz; 1 mT) also affected human periodontal ligament mesenchymal stem cells (PDLSCs) osteogenesis. Costantini et al. [48] proved that EMFs increased calcium deposition in cells and upregulated RUNX-2, COL1A1, and OPN expression.

An interesting study that used ASC-derived exosomes in osteopathist treatment, was performed by Xu et al. [78]. They reported that EMF exposure reduced inflammation and extracellular matrix degeneration in ASC-derived exosomes as well as increased COL2A1, SOX9, and ACAN expression in chondrocytes. Moreover, using the osteoarthritis rat model, authors showed that injecting EMF (75 Hz)-exposed ASC-derived exosomes promoted the regeneration of osteoarthritic cartilage [78]. A different study, performed by Sun et al. [79], also showed that static magnetic fields can increase COL2A1 and SOX9 expression and improve the migration of BM-MSCs through SDF-1/CXCR4. Additionally, Zhang et al. [13] showed that LF-EMFs can promote MSC migration by accumulating Ca${}^{2+}$ and through the FAK/Rho GTPase signaling pathways. In 2023, two studies investigated the effects of EMFs on MSCs cultured on hydrogel scaffolds and published the resulting chondrogenesis data. Both studies showed that EMFs can enhance chondrogenesis and this new tissue engineering approach (hydrogels and EMF) may increase the clinical potential of MSCs in treating cartilage defects [80, 81].

Studies have shown that EMFs have a positive effect on MSC differentiation and can improve as well as accelerate this process. Thus, EMFs represent an easy-to-apply tool that can be considered for use in stem cell therapy.