RESUMEN

Background: Recent advancements in basic medicine and epidemiology suggest a potential influence of blood pressure on scar formation, yet the specifics of this relationship are not fully understood. This study aims to clarify the causal link between blood pressure and the development of pathological scars using Mendelian randomization (MR). Methods: This study employed genetic variants closely linked to blood pressure as instrumental variables to explore the relationship between blood pressure and pathological scars. The inverse variance weighted (IVW) method was used for analysis. Results: Our analysis identified a notable association where higher blood pressure was correlated with a lower risk of pathological scars. Specifically, an increase in diastolic blood pressure (odds ratio [OR] per standard deviation increase: 0.67 [95% Confidence Interval [CI], 0.49-0.99]), systolic blood pressure (OR per standard deviation increase: 0.66 [95% CI, 0.46-0.93]), and hypertension (pooled OR: 0.39 [95% CI, 0.18-0.85]) were significantly associated with a reduced risk of keloids. Similarly, a genetic predisposition to hypertension (pooled OR: 0.31 [95% CI, 0.11-0.89]) was significantly associated with a reduced risk of hypertrophic scars. Neither reverse MR analysis nor Steiger's test indicated a significant reverse causal relationship between hypertension and either keloids or hypertrophic scars. Conclusion: The findings suggest a protective role of higher blood pressure against the development of pathological scars, including keloids and hypertrophic scars. However, the inconsistency observed across different MR methods warrants cautious interpretation and underscores the need for further investigation to confirm these findings.

RESUMEN

Background: Pathological scars, including keloids and hypertrophic scars, represent a significant dermatological challenge, and emerging evidence suggests a potential role for the gut microbiota in this process. Methods: Utilizing a two-sample Mendelian randomization (MR) methodology, this study meticulously analyzed data from genome-wide association studies (GWASs) relevant to the gut microbiota, keloids, and hypertrophic scars. The integrity and reliability of the results were rigorously evaluated through sensitivity, heterogeneity, pleiotropy, and directionality analyses. Results: By employing inverse variance weighted (IVW) method, our findings revealed a causal influence of five bacterial taxa on keloid formation: class Melainabacteria, class Negativicutes, order Selenomonadales, family XIII, and genus Coprococcus2. Seven gut microbiota have been identified as having causal relationships with hypertrophic scars: class Alphaproteobacteria, family Clostridiaceae1, family Desulfovibrionaceae, genus Eubacterium coprostanoligenes group, genus Eubacterium fissicatena group, genus Erysipelotrichaceae UCG003 and genus Subdoligranulum. Additional sensitivity analyses further validated the robustness of the associations above. Conclusion: Overall, our MR analysis supports the hypothesis that gut microbiota is causally linked to pathological scar formation, providing pivotal insights for future mechanistic and clinical research in this domain.

RESUMEN

Acne is a common chronic inflammatory dermatosis that can lead to pathological scars (PSs, divided into hypertrophic scars and keloids). These kinds of abnormal scars seriously reduce the quality of life of patients. However, their mechanism is still unclear, resulting in difficult clinical prevention, unstable treatment effects and a high risk of recurrence. Available evidence supports inflammatory changes caused by infection as one of the keys to abnormal proliferation of skin fibroblasts. In acne-induced PSs, increasing knowledge of the immunopathology indicates that inflammatory cells directly secrete growth factors to activate fibroblasts and release pro-inflammatory factors to promote the formation of PSs. T helper cells contribute to PSs via the secretion of interleukin (IL)-4 and IL-13, the pro-inflammatory factors; while regulatory T cells have anti-inflammatory effects, secrete IL-10 and prostaglandin E2, and suppress fibrosis production. Several treatments are available, but there is a lack of combination regimens to target different aspects of acne-induced PSs. Overall, this review indicates that the joint involvement of inflammatory response and fibrosis plays a crucial role in acne-induced PSs, and also analyzes the interaction of current treatments for acne and PS.

RESUMEN

The aim of this study was to investigate the effects of adiponectin (APN) on the proliferation and phenotypic transformation of human skin fibroblasts (HSFs) induced by TGF-ß1. Primary fibroblast cultures were collected from prepuce surgery, and the cell viability and proliferative activity of HSFs were detected by Cell Counting Kit-8 and EdU assays. In addition, cell migration was detected by Transwell assay. The protein levels of related genes in HSF were detected by Western blotting. The results showed that the proliferation and migration abilities of HSF in the TGF-ß1 group were significantly improved, and the relative protein expression levels of PCNA, α-SMA, and Collagen I in the TGF-ß1 group were greatly increased. Furthermore, TGF-ß1 stimulated the phosphorylation of p38 in HSF, while APN pretreatment significantly inhibited the TGF-ß1-induced phosphorylation of p38. Additionally, blocking the p38 MAPK signaling pathway relieved the injury in the HSF induced by TGF-ß1 and enhanced the therapeutic effect of APN in the TGF-ß1-treated HSF. In conclusion, APN inhibits TGF-ß1-induced HSF proliferation and myofibroblast phenotypic transformation by activating the p38 MAPK signaling pathway. APN is expected to become a potential target for preventing and treating skin fibrosis and pathological scars.

RESUMEN

The gut microbiome profile in patients with pathological scars remains rarely known, especially those patients who are susceptible to pathological scars. Previous studies demonstrated that gut microbial dysbiosis can promote the development of a series of diseases via the interaction between gut microbiota and host. The current study aimed to explore the gut microbiota of patients who are prone to suffer from pathological scars. 35 patients with pathological scars (PS group) and 40 patients with normal scars (NS group) were recruited for collection of fecal samples to sequence the 16S ribosomal RNA (16S rRNA) V3-V4 region of gut microbiota. Alpha diversity of gut microbiota showed a significant difference between NS group and PS group, and beta diversity indicated that the composition of gut microbiota in NS and PS participants was different, which implied that dysbiosis exhibits in patients who are susceptible to pathological scars. Based on phylum, genus, species levels, we demonstrated that the changing in some gut microbiota (Firmicutes; Bacteroides; Escherichia coli, etc.) may contribute to the occurrence or development of pathological scars. Moreover, the interaction network of gut microbiota in NS and PS group clearly revealed the different interaction model of each group. Our study has preliminary confirmed that dysbiosis exhibits in patients who are susceptible to pathological scars, and provide a new insight regarding the role of the gut microbiome in PS development and progression.

RESUMEN

BACKGROUND: Hyperbaric oxygen (HBO) therapy involves breathing pure oxygen or a high oxygen concentration above atmospheric (ATM) pressure in an enclosed chamber. Studies on pathological scars have demonstrated that HBO can inhibit the formation of pathological scars. OBJECTIVE: To evaluate the efficacy of HBO in the treatment of pathological scars via meta-analysis. METHODS: Searches were run on various databases, including the Cochrane, Embase, PubMed, Web of Science, and CNKI databases. A comparative study was conducted on patients with pathological scars treated with or without HBO. We used RevMan 5.4 software to determine the recurrence rate, treatment satisfaction, and Vancouver Scar Scale(VSS) score in the pathological scar. RESULTS: A total of 543 publications were identified; after screening, four were selected for review, including one randomized controlled trial (RCT), one controlled clinical trial (CCT), and two retrospective cohort studies. Meta-analysis results showed that HBO treatment reduced the pathological scar recurrence rate after surgery and radiotherapy (OR = 0.26, 95% CI: 0.13-0.52, p = 0.0001). Patients had higher satisfaction after HBO therapy (OR = 4.45, 95% CI: 1.49-13.30, p = 0.007). The Vancouver scar scale (VSS) score of patients with pathological scars was significantly improved in the HBO group (SMD: -3.82, 95% CI: -6.07to -0.49, p = 0.02). CONCLUSIONS: HBO treatment decreased the recurrence rate of pathological scars after surgery and radiotherapy, increased patient satisfaction, and reduced the VSS score, thus providing a new way to treat pathological scar hyperplasia. However, evaluation of the longer-term effects of HBO treatment requires further comprehensive studies, including more RCTs.

Asunto(s)

RESUMEN

BACKGROUND: Burn scars are a major clinical sequelae of severe burn wound healing. To effectively establish a successful treatment plan and achieve durable results, understanding the pathophysiology of scar development is of utmost importance. METHODS: A narrative review of the principles of the kinematic chain of movement and the hypothesised effect on burn scar development based on properties of burn scars was performed. An examination of the literature supporting these concepts is presented in conjunction with illustrative cases, with a particular focus on the effect of combination treatments that include ablative fractional resurfacing with surgical contracture releases. DISCUSSION: Ablative fractional resurfacing combined with the surgical release of contractures are an effective treatment modality for burn scar reconstruction. This treatment approach seems particularly effective because it is one of the only approaches where the principles of functional kinematics can be addressed when tailoring a reconstructive approach to an individual burn patient. The presented cases illustrate the importance of recognising and including the principles of functional kinematic chains in any reconstructive treatment approach for burn scars. Further, epifascial contracture bands are cord like structures which can be found underneath the subcutaneous fat of scar contractures which follow the principles of functional kinematics. Contractures can be more efficiently released if these structures are divided as well. CONCLUSION: Ablative fractional resurfacing combined with local tissue re-arrangements is a promising approach to address the underlying forces leading to hypertrophic burn scarring. To achieve an optimal outcome, it is essential to recognise and address the origin of the pathology when treating burn scars. Ablative fractional laser resurfacing allows a different scar approach as it is not limited to one surgical site and thus enables for effective treatment at the cause of the pathology.

Asunto(s)

RESUMEN

BACKGROUND: The endothelial-mesenchymal transition (EndMT) is an important mechanism in tissue regeneration and the development of organ fibrosis. Whether EndMT occurs in wound healing and scarring remains unknown. MATERIALS AND METHODS: The isolated cells from the normal dermal tissue and the wound tissue of mouse with full-thickness skin wound, and human scar tissue sections were performed with CD31/factorVII and α-SMA immunohistochemical staining and H and E staining. The ratio of factor VII or CD31/α-SMA double-positive cells in factor VII-positive cells was assessed in the isolated cells and in scar tissues. RESULTS: In this study, we found that approximately 27-60% of ECs coexpressed VII factor and α-SMA in the isolated cells from the wound tissues of mice, which was significantly higher than that of normal dermal tissue cells. Accordingly, the number of CD31/α-SMA double-positive cells in mouse wound tissue sections was also significantly more than that in normal dermal tissue sections. In scar tissues, in addition to high-density microvessels, a large number of proliferative ECs in scar strama and CD31/α-SMA double-positive cells were also found. Approximately 46.82 to 84.11% of ECs and 68.77 to 95.25% of myofibroblasts coexpressed VII factor and α-SMA, and these two values in hypertrophic scars were significantly higher than those in keloids. CONCLUSION: These results confirmed that ECs might contribute to the emergence of myofibroblasts in the wound and scar tissue via the process of EndMT.

Asunto(s)

RESUMEN

Introduction: The therapies of using exosomes derived from mesenchymal stem cells (MSC-Exo) for wound healing and scar attenuation and micro RNAs (miRNAs) for regulation of genes by translational inhibition and mRNA destabilization obtained great achievements. Silent information regulator 1 (SIRT1) is the silent information, which has an intricate role in many biological processes. However, the effects of SIRT1 and miR-138-5p loaded in MSC-Exo on pathological scars remain unclear. Methods: MSC-Exo was isolated and identified by ultracentrifugation, transmission electron microscopy, nanoparticle size measuring instrument and Western blot assays. The relationship between SIRT1 and miR-138-5p was verified by a double-luciferase reporter assay. Cell Counting Kit-8, Τranswell, scratch, and Western blot assays were used to evaluate the proliferation and migration of human skin fibroblasts (HSFs), and the protein expression of SIRT1, NF-κB, α-SMA and TGF-ß1 in HSFs, respectively. Flow cytometry was used to assess the apoptosis and cell cycle of HSFs affected by SIRT1. Results: Our study demonstrated that miR-138-5p loaded in MSC-Exo could attenuate proliferation, migration and protein expression of HSFs-derived NF-κB, α-SMA, and TGF-ß1 by targeting to SIRT1 gene, which confirmed the potential effects of MSC-Exo in alleviating pathological scars by performing as a miRNA's delivery vehicle. Conclusion: Exosomes derived from MSCs acting as a delivery vehicle to deliver miR-138-5p can downregulate SIRT1 to inhibit the growth and protein expression of HSFs and attenuate pathological scars.

Asunto(s)

RESUMEN

Introduction: Although bone marrow-derived mesenchymal stem cells (BMSCs) have attracted increasing attention because of their pivotal functions in the process of wound healing and fibrosis alleviation, the underlying molecular mechanisms have been poorly understood. Moreover, transforming growth factor beta 1 (TGF-ß1) is positively correlated with scar formation, whereas TGF-ß3 inhibits the pathological scar formation process. However, the relation of TGF-ß1, TGF-ß3, and the TGF-ß/Smad signaling pathway with BMSCs is unknown and requires further investigation. Methods: A cell co-culture platform was used to examine the relationship between BMSCs and dermal fibroblasts (DFs). EdU labelling and cell cycle detection were carried out to examine the viability of DF cells. Transwell and wound healing assays were used to test the cell migration of DFs. The expression of TGF-ß pathway components and collagens were determined by RT-qPCR and western blotting. A damaged skin rat model was applied to test the effects of BMSC treatment on skin wound healing. Results: The results showed that BMSC secretion could inhibit the viability and migration of DFs. Moreover, we observed that the TGF-ß-induced expression of TGF-ß1, Smad2, Smad3, COLI and COLIII was attenuated upon BMSC treatment in DFs, while the decrease in TGF-ß3 expression was enhanced by BMSCs. Furthermore, BMSC treatment accelerated wound healing and attenuated skin collagen deposition in a damaged skin rat model, leading to the mitigation of cell proliferation and enhancement of cell apoptosis. In addition, the expression of alpha-smooth muscle actin (α-SMA), COLI, and COLII was alleviated by BMSC treatment. Conclusions: Our results indicate that BMSCs can promote wound healing and inhibit skin collagen deposition, which is associated with the TGF-ß/Smad signaling pathway.

RESUMEN

OBJECTS: Keloids are intractable scar diseases and sometimes undergo hospitalization. This study aims to represent current status of keloid management in a national sample of hospitalized scar cases. METHODS: Data of scar-diagnosed cases admitted in 1064 China's tertiary hospitals between 2013 and 2018, were obtained from the Hospital Quality Monitoring System (HQMS) database. Variables analyzed include sex, age, nationality, occupation, hospital department, accompanied symptoms at admission, surgical treatment, length of stay (LOS), and hospitalization cost. The potential risk factors of keloid diagnosis among scar cases were preliminarily identified through the Cochran-Mantel-Haenszel tests and univariate regression analyses. RESULTS: This study identified 177,586 scar cases including 21,777 keloid cases and 155,809 non-keloid scar cases. The prevalence of scars in the HQMS database was gradually decreased from 0.123% in 2013 to 0.075% in 2018. We found a preponderances of males (54.32%), adults (61.52%), Han nationality (93.38%), and students (17.35%) in scar cases, among whom keloid cases accounted for growing proportions increasing from 9.2% in 2013 to 15.1% in 2018. Comparing non-keloid scar cases, keloid cases consisted of more women (59.1% VS 43.8%), office staffs (13.08% VS 6.75%) and retirees (5.16% VS 2.65%), and less Zhuang (0.79% VS 1.40%) and Hui nationalities (0.76% VS 1.00%), and showed lower incidence of accompanied symptoms (4.51% VS 47.96%) and higher rate of receiving operations (57.96% VS 50.28%, P < 0.001). Both the LOS and cost per hospitalization were lower in keloid cases. Furthermore, the adult and older women, Han and Uyghur nationalities, office staffs and retirees, and admitted in otolaryngology and dermatology departments, were potential predictors of keloid diagnosis among hospitalized scar cases. CONCLUSION: When viewed at the national level, keloid occupies an important part in scar management in Chinese tertiary hospitals. Demographic and clinical differences between keloids and other scars facilitate understanding and promoting of individualized anti-scar therapeutic strategies.

Asunto(s)

RESUMEN

AIMS: Norcantharidin (NCTD) exhibits antitumor, anti-inflammatory, and anti-fibrosis properties, which makes NCTD an attractive candidate for the treatment of pathological scars. This study was designed to investigate the potential effects of NCTD on fibroblast proliferation and explore the underlying mechanisms. MATERIALS AND METHODS: First, cell viability and cell apoptosis were evaluated to determine the effects of NCTD on human skin fibroblasts, at 10, 50, and 100 µM. To explore the mechanism, bioinformatics analyses, chromatin immunoprecipitation, RNA immunoprecipitation, and RNA pulldown assays, and luciferase reporter assays were performed to verify the relationships among NCTD, signal transducer and activator of transcription 3 (STAT3), annexin A2 pseudogene 2 (ANXA2P2), and ubiquitin-associated protein 2-like (UBAP2L) mRNA in fibroblasts. Loss-of-function experiments were performed to investigate the roles played by STAT3, ANXA2P2, and UBAP2L in the proliferation and apoptosis of fibroblasts. KEY FINDINGS: We found that NCTD administration induced fibroblast apoptosis and inhibited fibroblast proliferation in a dose-dependent manner. Mechanistically, NCTD inhibited ANXA2P2 transcription through the inhibition of STAT3 phosphorylation. Subsequently, ANXA2P2 was found to enhance the physical interaction between UBAP2L mRNA and lin-28 homolog B (LIN28B), which increased the stability and levels of UBAP2L mRNA. Loss-of-function assays demonstrated that ANXA2P2 and UBAP2L knockdown induced fibroblast apoptosis and suppressed fibroblast proliferation. SIGNIFICANCE: In conclusion, we confirmed that NCTD inhibits fibroblast proliferation by inhibiting the STAT3/ANXA2P2/UBAP2L axis, which suggested that NCTD could represent a new candidate for the treatment of pathological scars.

Asunto(s)

RESUMEN

This is a transverse and retrospective descriptive study carried out on a quantitative and qualitative component on pathological scars after a second ear piercing for aesthetic purposes in a Negroid female population from an endemic area of keloids. For a period of 10 years (from January 1, 2010 to December 31, 2019), we observed 172 patients with pathological ear scars after a second piercing for aesthetic purposes including 65.7% of female students and 22.1% of students. Clinically, we had 143 (83.1%) patients with keloids and 29 (16.9%) with hypertrophic scars. The average age of the second piercing was 22.62 years; 98 (57%) patients had single lesions on the pierced ear and 74 (43%) multiple lesions; 168 (97.7%) had no family history of pathological scars. Our patients from an endemic area of keloids did not develop pathological scars during the first piercing but all develop pathological scars after the second piercing. Several risk factors could be accused: heredity, environment, race, age, gender, wearing of poor-quality jewelry, infection, disruption of the healing process caused by the first piercing, mechanical tension caused by the new ornamental object. However, none of these assumptions has been verified. In the meantime, we do not recommend that at risk negroid subjects, originating from areas with high endemicity of keloids, a second ear piercing for aesthetic purposes.

Asunto(s)

RESUMEN

Soft tissue fibrosis in important organs such as the heart, liver, lung, and kidney is a serious pathological process that is characterized by excessive connective tissue deposition. It is the result of chronic but progressive accumulation of fibroblasts and their production of extracellular matrix components such as collagens. Research on pathological scars, namely, hypertrophic scars and keloids, may provide important clues about the mechanisms that drive soft tissue fibrosis, in particular the vascular involvement. This is because these dermal fibrotic lesions bear all of the fibrotic characteristics seen in soft tissue fibrosis. Moreover, their location on the skin surface means they are readily observable and directly treatable and therefore more accessible to research. We will focus here on the roles that blood vessel-associated cells play in cutaneous scar pathology and assess from the literature whether these cells also contribute to other soft tissue fibroses. These cells include endothelial cells, which not only exhibit aberrant functions but also differentiate into mesenchymal cells in pathological scars. They also include pericytes, hepatic stellate cells, fibrocytes, and myofibroblasts. This article will review with broad strokes the roles that these cells play in the pathophysiology of different soft tissue fibroses. We hope that this brief but wide-ranging overview of the vascular involvement in fibrosis pathophysiology will aid research into the mechanisms underlying fibrosis and that this will eventually lead to the development of interventions that can prevent, reduce, or even reverse fibrosis formation and/or progression.

Asunto(s)

RESUMEN

There has been a long-standing need for guidelines on the diagnosis and treatment of keloids and hypertrophic scars that are based on an understanding of the pathomechanisms that underlie these skin fibrotic diseases. This is particularly true for clinicians who deal with Asian and African patients because these ethnicities are highly prone to these diseases. By contrast, Caucasians are less likely to develop keloids and hypertrophic scars, and if they do, the scars tend not to be severe. This ethnic disparity also means that countries vary in terms of their differential diagnostic algorithms. The lack of clear treatment guidelines also means that primary care physicians are currently applying a hotchpotch of treatments, with uneven outcomes. To overcome these issues, the Japan Scar Workshop (JSW) has created a tool that allows clinicians to objectively diagnose and distinguish between keloids, hypertrophic scars, and mature scars. This tool is called the JSW Scar Scale (JSS) and it involves scoring the risk factors of the individual patients and the affected areas. The tool is simple and easy to use. As a result, even physicians who are not accustomed to keloids and hypertrophic scars can easily diagnose them and judge their severity. The JSW has also established a committee that, in cooperation with outside experts in various fields, has prepared a Consensus Document on keloid and hypertrophic scar treatment guidelines. These guidelines are simple and will allow even inexperienced clinicians to choose the most appropriate treatment strategy. The Consensus Document is provided in this article. It describes (1) the diagnostic algorithm for pathological scars and how to differentiate them from clinically similar benign and malignant tumors, (2) the general treatment algorithms for keloids and hypertrophic scars at different medical facilities, (3) the rationale behind each treatment for keloids and hypertrophic scars, and (4) the body site-specific treatment protocols for these scars. We believe that this Consensus Document will be helpful for physicians from all over the world who treat keloids and hypertrophic scars.

RESUMEN

Burn wounds are a global public health problem, which affects all countries, no matter the development stage and occurs in all age groups, from toddlers to elderly. In spite of burns being the cause of numerous household and work accidents, there are still no clear stated unanimous rules for their treatment. Every day new products appear on the market, each of them trying to prove more effective. Since ancient times, silver has been known for its antimicrobial properties, so it has been used for a long time in the treatment of burns and other types of wounds. One of the relatively modern methods of treatment is applying silver sheets on the scald lesions. In this paper, which was part of a larger study (research for a PhD thesis), concerning prevention and treatment of the post-burn pathological scars, the cases of some patients with burns, who were treated by using the above mentioned method were presented and analyzed. The results obtained by applying silver sheets were then commented and interpreted, pointing out the advantages and disadvantages compared to silver sulfadiazine creams and ointments, which have already been used at a large scale. The prevention and treatment of post-burn pathological (hypertrophic and keloid) scars is a field in which still little is known and in which there are also no clearly set therapy plans. We hope that through this research and the following ones we will manage to establish some major guidelines concerning the prevention of pathological scars, which are not only disabling, but also a major aesthetic issue for any patient, in order to obtain better outcomes.

Asunto(s)

RESUMEN

Scar formation is a consequence of the wound healing process that occurs when body tissues are damaged by a physical injury. Hypertrophic scars and keloids are pathological scars resulting from abnormal responses to trauma and can be itchy and painful, causing serious functional and cosmetic disability. The current review will focus on the definition of hypertrophic scars, distinguishing them from keloids and on the various methods for treating hypertrophic scarring that have been described in the literature, including treatments with clearly proven efficiency and therapies with doubtful benefits. Numerous methods have been described for the treatment of abnormal scars, but to date, the optimal treatment method has not been established. This review will explore the differences between different types of nonsurgical management of hypertrophic scars, focusing on the indications, uses, mechanisms of action, associations and efficacies of the following therapies: silicone, pressure garments, onion extract, intralesional corticoid injections and bleomycin. .

Asunto(s)

RESUMEN

Pathological scars are fibroproliferative skin disorders that are characterised by the accumulation of fibroblasts and collagens. It is increasingly understood that their development and progression may be related to local skin mechanics, such as stretching. The present study evaluated the morphological and functional effects of cellular stretch on normal human dermal fibroblasts and explored the mechanotransduction mechanisms that may be involved. When fibroblasts were subjected to 24 h of cyclic axial stretching (10 cycles min(-1)), they migrated faster and for a longer distance than unstretched cells. The increased migration resulted in the cells reorienting themselves perpendicular to the direction of stretching. This was associated with reduced cellular apoptosis and unchanged proliferation. Stretching did not increase collagen synthesis but did elevate collagen degradation. These biological effects appeared to be mediated by the integrin and Wnt mechanotransduction pathways, which transmitted the mechanical stimulus via cell-substrate interactions, cell-cell junctions and indirect cell-cell communications. A better understanding of such fibroblast mechanoresponses in vitro will help the development of novel interventions that can prevent, reduce or even reverse pathological scar formation and/or progression in vivo.

Asunto(s)