Jian-Guo Feng, PhD, Associate Professor, Principal Investigator, Department of Anesthesiology, The Affiliated Hospital, Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. fengjianguo@swmu.edu.cn
Research Domain of This Article
Dermatology
Article-Type of This Article
editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Chun-Yi Wu, Xie-Hua Xiao, Jian-Guo Feng, Department of Anesthesiology, The Affiliated Hospital, Southwest Medical University, Luzhou 646000, Sichuan Province, China
Author contributions: Wu CY and Xiao XH contributed to writing-original draft, have made crucial and indispensable contributions towards the completion of the project and thus qualified as the co-first authors of the paper; Wu CY contributed to visualization and software; Feng JG contributed to conception and design of the study, manuscript review and editing; all authors contributed to the manuscript and approved the submitted version.
Supported by Sichuan Science and Technology Program, No. 2025ZNSFSC0744; Health Commission of Sichuan Province Medical Science and Technology Program, No. 24QNMP040; and Luzhou Science and Technology Program, No. 2025RCX002.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Corresponding author: Jian-Guo Feng, PhD, Associate Professor, Principal Investigator, Department of Anesthesiology, The Affiliated Hospital, Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. fengjianguo@swmu.edu.cn
Received: December 2, 2025 Revised: January 14, 2026 Accepted: February 4, 2026 Published online: September 15, 2026 Processing time: 276 Days and 19.5 Hours
Abstract
Chronic diabetic wounds represent a significant burden on global healthcare, characterized by their refractory nature and high risk of lower-limb amputation, which is mainly attributed to impaired angiogenesis and persistent endothelial dysfunction in a hostile hyperglycemic microenvironment. Mesenchymal stem cell-derived exosomes (MSC-Exos) have emerged as promising cell-free therapeutic options; however, their baseline bioactivity is often insufficient to achieve consistent clinical efficacy. Chen et al recently published a study in World Journal of Diabetes showing that fractional carbon dioxide (CO2) laser-based photothermal preconditioning of adipose-derived MSCs enhances the pro-angiogenic activity of Exos by enriching sphingosine-1-phosphate (S1P) cargo and activating endothelial S1P receptor 1/protein kinase B/hypoxia-inducible factor-1α signaling. In this editorial, we position these findings within the broader context of Exo engineering and preconditioning strategies for diabetic wound repair. We also highlight the conceptual distinction among physical, pharmacological and genetic preconditioning approaches, and discuss the specific advantages of fractional CO2 laser as a drug-free, dose-tunable and clinically familiar platform to enhance the functional potency and cargo composition of Exos rather than simply increase total Exos yield. We further outline key translational issues that remain to be addressed, including donor heterogeneity, parameter and dose standardization, and the integration of laser preconditioning into scalable good manufacturing practice compliant Exo production workflows. Overall, clinically available fractional CO2 laser systems offer a uniquely controllable preconditioning modality that can bridge the gap between promising preclinical data and real-world applications of MSC-Exos in diabetic wound healing, provided that their safety, reproducibility and long-term vascular effects are rigorously evaluated.
Core Tip: This editorial highlight that fractional carbon dioxide (CO2) laser pre-conditioning offers a novel, drug-free strategy to enhance the therapeutic quality of adipose-derived mesenchymal stem cell exosomes (Exos) for diabetic wound repair. We emphasize recent findings that this physical pre-conditioning strategy, utilizing clinically established and dose-tunable photothermal stimulation, enriches sphingosine-1-phosphate (S1P) cargo and activates endothelial S1P receptor 1/protein kinase B/hypoxia-inducible factor-1α signaling, thereby promoting improved angiogenesis and cytoprotection. This concept reframes fractional CO2 lasers as a scalable, good manufacturing practice-compatible platform to “upgrade” Exos bioactivity for chronic diabetic wounds.
This editorial refers to “Fractional carbon dioxide laser-induced photothermal activation of mesenchymal stem cell-derived exosomes accelerates diabetic wound healing by enhancing angiogenesis” by Chen et al, 2026; https://doi.org/10.4239/wjd.v17.i1.112942.
INTRODUCTION
Chronic non-healing wounds are among the most debilitating complications of diabetes driven by a pathological triad of persistent endothelial dysfunction, impaired angiogenesis, and chronic inflammation[1,2]. Collectively, these abnormalities compromise oxygen and nutrient delivery, thereby predisposing patients with diabetic foot ulcers to high rates of infection and limb amputation[3]. Over the past decade, mesenchymal stem cells (MSCs) have been extensively investigated as regenerative agent for these lesions. Nevertheless, a paradigm shift has emerged: Therapeutic benefits of MSCs are mediated predominantly via paracrine mechanisms, with extracellular vesicles (EVs), particularly exosomes (Exos), a specific EV subtype of endosomal origin that typically ranges from approximately 30 nm to 150 nm in diameter, playing a central role[4,5].
MSC-derived Exos (MSC-Exos) are acellular nanovesicles exerting therapeutic effects on chronic diabetic wounds via coordinated molecular mechanisms rather than direct cell replacement. By delivering bioactive cargo, including microRNAs (miRNAs), mRNAs, proteins, lipids, and metabolites, to recipient cells via endocytosis, membrane fusion, or receptor engagement, these Exos reprogram intracellular signaling and gene expression[6,7]. Mechanistically, in diabetic wounds, MSC-Exos modulate immune responses by shifting macrophage polarization from a persistent pro-inflammatory M1-like state to a pro-resolution M2-like phenotype, thereby attenuating chronic inflammation[8]. Furthermore, they enhance angiogenesis by transferring pro-angiogenic factors and regulatory miRNAs to endothelial cells[9], stimulate fibroblast proliferation and constructive extracellular matrix (ECM) remodeling, and accelerate keratinocyte migration to support re-epithelialization[10]. These Exos also mitigate oxidative stress in a hyperglycemic microenvironment[11]. Overall, MSC-Exos address critical barriers in diabetic wound management by promoting functional skin restoration via the intricate modulation of angiogenesis, immunoregulation, oxidative stress, ECM remodeling, and re-epithelialization.
MSC-Exos exhibit distinct advantages, such as lower immunogenicity, better stability, and a reduced risk of tumorigenesis, over whole-cell therapy. Preclinical evidence suggests that Exos from various sources, including adipose-derived-MSCs (Ad-MSCs), human umbilical cord-derived-MSCs, and bone marrow-derived-MSCs (BM-MSCs), facilitate cutaneous wound healing by regulating inflammation, angiogenesis, and re-epithelialization and enhancing collagen deposition[12]. MSC-Exos carry proteins, lipids, mRNAs, and non-coding RNAs that reprogram recipient cells, modulate inflammation, and promote angiogenesis, collectively facilitating wound healing[6,7]. Despite these promising effects, the intrinsic pro-angiogenic activity of naive MSC-Exos is often variable and suboptimal in a refractory diabetic wound environment. Consequently, the field has moved toward “exosome engineering” to tune the cargo and functions of Exos via MSC preconditioning[13].
Chen et al[14] recently published a study in World Journal of Diabetes introduced a novel physical preconditioning strategy using low-energy fractional carbon dioxide (CO2) laser to potentiate Ad-MSC-Exos. They found that photothermal stimulation (40 mJ/cm2) upregulated heat shock protein-90 levels and enriched sphingosine-1-phosphate (S1P) cargo within Exos. Mechanistically, these laser-activated Exos enhanced endothelial angiogenesis via the S1P receptor 1/protein kinase B (AKT)/hypoxia-inducible factor (HIF-1α) signaling axis, effectively reversing high-glucose-induced endothelial dysfunction. In vivo, this approach accelerated diabetic wound closure and neovascularization, serving as a promising non-invasive method to optimize cell-free therapeutics for chronic wound management.
DIABETIC WOUNDS AND THE RISE OF CELL-FREE MSC THERAPIES
Diabetic wounds are characterized by persistent inflammation, impaired angiogenesis, keratinocyte and fibroblast dysfuction, and increased oxidative stress. Cell-free MSC-based therapies, which rely on MSC-derived products, directly target these pathological features. Specifically, MSC-derived Exos and EVs are the most extensively investigated modalities for cutaneous wound repair and have been generated from multiple MSC sources, including Ad-MSCs[15], umbilical cord-derived MSCs (UC-MSCs)[16], human BM-MSCs[17], and fetal dermal MSCs[18,19]. Other MSC-derived products such as apoptotic bodies (ABs)[20] and conditioned medium (CM)[21,22] also promote skin wound healing (Table 1)[23-28].
ApoSEVs facilitate macrophages polarization from M1 to M2, enhance endothelial cell proliferation, migration, and tube formation, and stimulate fibroblast proliferation and migration
Diabetic wounds exhibit a persistent, dysregulated inflammatory milieu that is qualitatively distinct from the self-limiting inflammation observed during normal healing[29,30]. Neutrophil infiltration is prolonged, with sustained release of reactive oxygen species (ROS) and proteases that damage ECM and degrade growth factors. Simultaneously, macrophage dynamics are disrupted, characterized by an impaired transition from pro-inflammatory (M1-like) to reparative (M2-like) phenotypes, reduced efferocytosis, and chronic NLR family pyrin domain-containing 3 inflammasome activation, which collectively sustain interleukin-1β/tumor necrosis factorα production and matrix degradation[31]. Hyperglycemia-driven advances glycation end product accumulation and defective angiogenesis further reinforce this feed-forward loop, ultimately delaying re-epithelialization and matrix deposition. In this context, immunomodulation is a pivotal advantage of MSC-derived cell-free products for managing chronic diabetic inflammation and wound repair. In addition to the well-established roles of MSC-Exos and EVs, MSC-derived ABs (MSC-ABs) and apoptotic small EVs (apoSEVs) exhibit a potent ability to reprogram the hostile M1-dominant inflammatory milieu typical of diabetic wounds into a pro-healing environment. Previous studies on C57BL/6 mice indicated that BM-MSC-ABs drive M0 macrophages toward an M2 phenotype, thereby regulating inflammation and angiogenesis to accelerate healing[20], while simultaneously enhancing fibroblast migration and proliferation via these functionally converted macrophages[28]. Similarly, in diabetic db/db mice, apoSEVs from Ad-MSCs facilitate the M1-to-M2 switch, stimulating endothelial tube formation and fibroblast activity[27]. Complementing these vesicular mechanisms, MSC secretome and CM provide a soluble, multifactorial approach for tissue regeneration. For instance, the secretome from human deciduous pulp MSCs modulates inflammatory responses in keratinocytes[21]. Furthermore, CM from human umbilical cord Wharton’s jelly stem cells effectively treats both excisional and diabetic wounds in vascular endothelial growth factor and db/db mice by fostering keratinocyte differentiation and releasing key therapeutic molecules[29]. Therefore, diverse MSC-derived cell free therapeutics-including apoptotic vesicles and soluble secretomes, warrant further investigation, as they effectively overcome the intrinsic cellular dysfunction in diabetic skin by delivering coordinated immunoregulatory, pro-angiogenic, and pro-epithelial signals.
Defective clearance of cellular debris, ECM fragments, and metabolic waste is increasingly recognized as a central mechanism driving chronicity in diabetic wounds. Emerging evidence suggests that MSC-Exos reverse these deficits by delivering bioactive cargoes that restore macrophage efferocytosis and reactivate autophagic flux, thereby actively clearing the toxic microenvironment to facilitate the transition from inflammation to proliferation. Specifically, MSCs secrete MFG-E8, which reduces tumor necrosis factor-α production and enhances the phagocytic clearance of apoptotic cells[32]. Furthermore, MSC-Exos enriched with miR-223 target Pknox1 to promote M2 macrophage polarization, thereby boosting their phagocytic capacity[8]. Regarding intracellular clearance, Ad-MSC-Exos modified with mmu_circ_0000250 restore defective autophagic flux via the miR-128-3p/sirtuin axis, concurrently promoting angiogenesis and tissue survival[33].
Taken together, the studies summarized in Table 1 offer a coherent mechanistic rationale and preclinical foundation for the application of MSC derived Exos, EVs, ABs, apoSEVs, and CM in diabetic wound healing. These cell free products integrate multiple key processes, including angiogenesis promotion, ferroptosis and fibrosis modulation, reepithelialization, ECM normalization, and macrophage reprogramming, which are disrupted in diabetic ulcers. Their acellular nature not only reduces tumorigenic and immunologic risks but also facilitates scalable manufacturing and storage. Moreover, they are compatible with advanced dressings and delivery systems, making cell free MSC therapies as highly promising translational candidates for diabetic wound management. Future studies should explore novel methods to further improve the quality of MSC-derived products.
PRECONDITIONING STRATEGIES: TUNING EXO QUALITY, NOT JUST QUANTITY
Preconditioning, also known as priming or licensing, is used to optimize the adaptive responses of a cell population to a pathological environment. This approach was first described in 1986 by Reimer et al[34] in the context of myocardial ischemia[35]. It involves exposing cells to specific stimuli to enhance their resilience and secretory capacity. In the context of MSC therapy, this concept is also known as programmable biologics, in which the cargo and functions can be deliberately “tuned” via preconditioning. This approach allows MSCs to counteract hostile disease environments, such as glucotoxicity in type 2 diabetes, by activating protective survival pathways and improving the bioactivity of their vesicular payloads[36-41].
Current enhancement strategies primarily rely on pharmacological preconditioning to augment the immunomodulatory and angiogenic potential of MSC-Exos (Table 2)[42-44]. For instance, pretreatment with antidiabetic agents, such as pioglitazone[35] and empagliflozin[37] drastically increases the exosomal angiogenic cargo, accelerating diabetic wound closure. Similarly, statins such as atorvastatin promote endothelial function and wound repair[38]. In addition to synthetic drugs, natural compounds also show high efficacy. For example, quercetin-preconditioned MSC-Exos significantly enhance fibroblast proliferation[39], Curcumin priming promotes epithelial migration and collagen deposition[40]. Furthermore, rapamycin-primed small EVs (sEVs) exhibit exceptional efficacy in modulating the immune microenvironment by driving M1-to-M2 macrophage polarization[16]. However, despite its potential, pharmacological priming raises significant translational concerns regarding residual drug traces, off-target effects, and regulatory complexities.
RAPA-sEVs effectively accelerate wound repair by promoting angiogenesis, reducing M1-type macrophages, and suppressing excessive inflammation with high biosafety
These above-mentioned limitations have created a niche for physical preconditioning methods, which use biophysical stimuli to enhance EV yield and functionality without introducing exogenous chemical agents. Hypoxic preconditioning is the most well-established physical strategy. By mimicking the low-oxygen tension of the stem cell niche, hypoxia-pretreated MSC-derived sEVs accelerate diabetic wound healing by transferring miR-17-5p, which targets the toll-like receptor-4/ROS/mitogen-activated protein kinase pathway to suppress excessive neutrophil extracellular trap formation[41]. In addition to hypoxia, emerging physical modalities such as light, sound, and mechanical forces offer promising yet underexplored avenues for EV engineering. For example, blue light illumination (455 nm) significantly enhances the pro-angiogenic potential of umbilical cord MSC-Exos in burn models[43]. Moreover, we have previously found that mechanical stimuli induce cell proliferation and specific growth factor release[45]. MSCs are inherently mechanosensitive and dynamically respond to their physical microenvironment. Cues such as stiffness, viscoelasticity, and mechanical forces intricately regulate their fate, secretory profile, and paracrine signaling[46]. Recently, Kang et al[47] demonstrated that biomaterial-derived mechanical stimuli play a pivotal role in shaping the therapeutic potential of MSC-derived EVs. These MSC-derived EVs demonstrated unique angiogenic and immunomodulatory activities, influenced by the mechanical properties of the biomaterial used. Consistently, mechanical stretch enhances the secretion of pro-healing factors such as macrophage colony-stimulating factor[45], suggesting that mechanical stimulation is an effective preconditioning strategy to optimize MSC secretome bioactivity. Similarly, low-intensity pulsed ultrasound not only promotes neurogenesis and angiogenesis in refractory foot ulcers[44] but also stimulates Exo secretion[48]. Electrical stimulation (ES) is an important physical cue that alters the membrane potential and activates specific voltage-gated ion channels, thereby modulating MSC proliferation, migration, and differentiation[49,50]. However, the mechanisms by which ES influences the composition and functional potential of MSC-derived secretomes and EVs remain unclear. Recently, Zhang et al[51] reported that specific directcurrent ES enhances the secretion of cardioprotective EVs from cardiac MSCs. Similarly, the magnetic stimulation enhances the MSC angiogenic potential[52] and release of Exos[53]. These findings highlight ES and magnetic stimulation as viable strategies to modulate MSC bioactivity and the therapeutic potential of their secretomes. Optimization of these physical preconditioning strategies may provide effective cues for future clinical applications of MSC-derived products by enhancing their yield and biological cargo. In summary (Figure 1), currently, to enhance their therapeutic potential, MSCs are subjected to two main categories of pre-conditioning strategies: (1) Physical stimuli, including blue light radiation, electrical and magnetic stimulation, hypoxia, fractional CO2 laser, ultrasound, and mechanical stimuli; and (2) Pharmacological agents, such as quercetin, curcumin, flavonoids, rapamycin, pioglitazone, empagliflozin, and atorvastatin. These interventions potentiate the secretion of bioactive products, including EVs, Exos, ABs, and CM. Administration of these pre-conditioned secretomes accelerates wound healing.
Figure 1 Schematic illustration of pre-conditioning strategies to enhance mesenchymal stem cells-derived secretomes for cutaneous wound healing.
Mesenchymal stem cells (MSCs) are isolated from diverse tissue sources, including the umbilical cord, adipose tissue, bone marrow, and dermal tissue. To augment their therapeutic potential, MSCs are subjected to two main categories of pre-conditioning strategies: (1) Physical stimuli, including blue light radiation, electrical and magnetic stimulation, hypoxia, fractional carbon dioxide laser, ultrasound, and mechanical stimuli; and (2) Pharmacological agents, such as quercetin, curcumin, flavonoids, rapamycin, pioglitazone, empagliflozin, and atorvastatin. These interventions potentiate the secretion of bioactive products, including extracellular vesicles, exosomes, apoptotic bodies, and conditioned medium. Administration of these pre-conditioned secretomes accelerates wound healing by promoting extracellular matrix remodeling, angiogenesis, hair follicle regeneration, re-epithelialization, fibroblast proliferation/migration, and macrophage polarization. MSC: Mesenchymal stem cells; CO2: Carbon dioxide.
In this study, Chen et al[14] demonstrated that low-energy fractional CO2 laser irradiation, an innovative physical preconditioning strategy for MSCs, enhances the biological activity of MSC-Exos via photothermal stimulation. These Exos, subsequently promote endothelial cell function by activating the S1PR1/AKT/HIF1α signaling axis, thereby accelerating diabetic wound repair. As CO2 lasers are widely used for cutaneous indications and exhibit a well characterized safety profile[54], leveraging existing clinical devices and parameter settings can substantially shorten the translational pathway from laboratory protocols to Good Manufacturing Practice-compliant manufacturing, highlighting both the safety and the clinical translatability of this approach.
Although the manuscript presents meaningful findings, it does not sufficiently address the limitations and translational challenges of Exo-based therapies for diabetic wound repair. Despite encouraging preclinical evidence, several limitations remain. First, Exo preparations are intrinsically heterogeneous and strongly affected by the cell source and culture conditions. However, definitive subtype attribution and standardized, mechanism-linked potency assays are currently lacking, undermining reproducibility, dose selection, and cross-study comparability[55]. Second, scalable, good manufacturing practice-compliant manufacturing and rigorous quality-control frameworks (including identity, purity, and stability specifications) have not yet been fully established, increasing the risk of batch-to-batch variability. Third, after local or systemic administration, Exos may be rapidly cleared or show limited retention and bioavailability in the protease- and ROS-rich chronic wound microenvironment, necessitating the development of optimized delivery systems and robust pharmacokinetic/pharmacodynamic evaluation. Finally, safety and regulatory issues-including off-target bioactivity, potential immunogenicity or procoagulant effects, and the need for long-term risk assessment—must be systematically addressed to facilitate clinical translation[56].
Importantly, evaluation of the therapeutic efficacy of Exo-based interventions, particularly preconditioned MSC-Exos , should explicitly incorporate patient-specific factors and comorbidities that often dominate wound-healing outcomes, including glycemic control, infection burden, biofilm formation, tissue perfusion/ischemia (e.g., peripheral arterial disease), neuropathy, adherence to pressure offloading, chronic kidney disease, obesity, malnutrition, aging, smoking status, and concomitant medications. These variables modulate inflammation, angiogenesis, ECM remodeling, and cellular responsiveness, thereby affecting both baseline healing trajectories and the apparent magnitude of benefits of Exo therapy. Therefore, stratified enrollment and pre-specified subgroup analyses based on these clinical determinants are crucial to accurately identify responders and optimize treatment regimens in diabetic wound trials[55].
THERAPEUTIC IMPLICATIONS AND FUTURE DIRECTIONS
Chen et al[14] demonstrated that low-energy fractional CO2 laser irradiation enhances the exosomal pro-angiogenic and cytoprotective activities of Ad-MSCs by enriching S1P and activating the S1PR1/AKT/HIF-1α signaling pathway in endothelial cells. However, further comprehensive dissection of exosomal cargo is necessary. Future studies should use integrated multi-omics platforms, including lipidomics, proteomics, and transcriptomics/miRNomics, to map the full spectrum of laser-induced alterations in exosomal contents. Such analyses may reveal additional bioactive lipids, chaperones, cytokines, and non-coding RNAs that jointly drive angiogenesis, immunomodulation, and cytoprotection. Simultaneously, a systematic characterization of the broader MSC secretome (CM beyond Exos) is crucial to elucidate the mechanisms by which CO2 laser preconditioning reshapes the paracrine milieu. Insights derived from these studies can guide the development of rational engineering strategies. For instance, particularly beneficial factors can be selected or overexpressed and CO2 laser preconditioning can be combined with genetic modifications (e.g., enforced S1P overexpression in MSCs) to further enhance therapeutic potency in a controlled manner.
Whether the observed effects are conserved across MSC sources and donor backgrounds or MSC type-dependent warrants further investigation. This article focused on Ad-MSCs from a restricted donor pool. Nevertheless, BM-MSCs, UC-MSCs, and other tissue-specific MSCs may exhibit distinct stress responses, exosomal profiles, and therapeutic efficacy after CO2 laser exposure. Therefore, systematic comparisons of various MSC types are essential to identify the most responsive and clinically relevant cell source. Additionally, donor-related variables, such as sex, age, metabolic status, and comorbidities, are particularly relevant in the context of diabetic wound healing, as sex-related differences have been reported in cutaneous repair[57]. Future studies should use larger, sex-balanced, and metabolically diverse donor cohorts to clarify the mechanisms by which these factors influence the magnitude and quality of exosomal responses to laser preconditioning and ensure that the resultant products are widely applicable and effective across patient subgroups.
Finally, long-term safety and off-target effects must be rigorously evaluated before widespread clinical adoption. Although Exos are generally considered to be safer than live-cell therapies, the intentional enhancement of pro-angiogenic and pro-survival pathways raises theoretical concerns regarding potential tumor angiogenesis, abnormal vascular remodeling, or exacerbation of proliferative dermatoses in susceptible individuals. Therefore, long-term in vivo studies using both diabetic and non-diabetic models should be performed to characterize the biodistribution, persistence, clearance kinetics, and potential off-target vascular or immunological effects of CO2 laser-preconditioned MSC-Exos. Moreover, these studies should ideally be supplemented with tumor-prone or oncogene-sensitized models to formally rule out pro-tumorigenic risks. Collectively, the clinical familiarity and safety of CO2 lasers, along with appropriate mechanistic, standardization, and safety studies, make CO2 laser preconditioning a highly promising and rapidly translatable strategy for the development of robust cell-free Exo therapies for various pathologies, including diabetic wound complications.
CONCLUSION
The work by Chen et al[14] indicates that fractional CO2 laser preconditioning, an innovative physical preconditioning strategy, reprograms Ad-MSC-Exos into S1P-enriched pro-angiogenic vesicles. These modified Exos can mitigate endothelial dysfunction and accelerate diabetic wound healing. This approach offers a potentially distinct and clinically feasible strategy for Exo-based regeneration. Unlike pharmacological and genetic methods, fractional CO2 laser uses an established and precisely controllable clinical technology to potentially enhance Exo quality without exogenous agents. Therefore, this work bridges the fields of laser-based skin repair and MSC-Exo therapy, outlining a practical path toward combined or sequential interventions for chronic diabetic wounds.
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P-Reviewer: Qian YX, MD, Researcher, China; Wu SZ, MD, Professor, China; Xu HJ, Adjunct Professor, Associate Professor, PhD, Postdoc, China S-Editor: Liu H L-Editor: A P-Editor: Wang CH
