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Endomysium
Endomysium
Endomysium
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Endomysium
Structure of a skeletal muscle. (Endomysium labeled at bottom center.)
Identifiers
TA98A04.0.00.043
TA22007
THH3.03.00.0.00004
FMA9729
Anatomical terminology

The endomysium, meaning within the muscle, is a wispy layer of areolar connective tissue that ensheaths each individual muscle fiber, or muscle cell.[1][2][3] It also contains capillaries and nerves. It overlies the muscle fiber's cell membrane: the sarcolemma. Endomysium is the deepest and smallest component of muscle connective tissue. This thin layer helps provide an appropriate chemical environment for the exchange of calcium, sodium, and potassium, which is essential for the excitation and subsequent contraction of a muscle fiber.

Endomysium combines with perimysium and epimysium to create the collagen fibers of tendons, providing the tissue connection between muscles and bones by indirect attachment.[4] It connects with perimysium using intermittent perimysial junction plates.[5]

Collagen is the major protein that composes connective tissues like endomysium.[6] Endomysium has been shown to contain mainly type I and type III collagen components, and type IV and type V in very minor amounts.[7] Others have found type IV and type V more common.[2]

The term cardiac skeleton is sometimes considered synonymous with endomysium in the heart, but cardiac skeleton also refers to the combination of the endomysium and perimysium.[citation needed]

Clinical significance

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Anti-endomysial antibodies (EMA) are present in celiac disease.[8] They do not cause any direct symptoms to muscles, but detection of EMA is useful in the diagnosis of the disease.[9]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Endomysium

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from Grokipedia
The endomysium is the thin, innermost layer of that surrounds each individual muscle fiber, providing essential structural support and protection within the muscle's fascicles. While most commonly associated with , endomysium is also present in cardiac and , surrounding individual muscle fibers. Composed primarily of loose areolar , including and reticular fibers, the endomysium also contains and nutrients that surround the muscle fiber to aid its metabolic needs. This delicate sheath encases the fragile muscle fibers, helping them withstand the mechanical stresses of contraction without damage. In terms of function, the endomysium serves as a conduit for capillaries, vessels, and fibers, enabling the delivery of oxygen and nutrients to the muscle fiber while facilitating the removal of products. It forms part of the muscle's microvascular network, with terminal arterioles branching into capillaries that permeate this layer to supply blood directly to the fibers. Within the hierarchical organization of , the endomysium represents the finest level of , surrounding single fibers that bundle into fascicles enveloped by perimysium and the entire muscle covered by . This arrangement ensures coordinated force transmission and maintains the overall integrity of the muscle during movement.

Anatomy

Definition and Location

The endomysium is defined as a thin layer of areolar that directly ensheaths each individual fiber, also known as a myofiber. This delicate sheath provides immediate structural support to the fiber while allowing flexibility during contraction. Anatomically, the endomysium surrounds every single muscle fiber within a , forming a continuous network that extends from the muscle's origin to its insertion along the entire length of the fiber. It lies innermost among the muscle's connective tissue layers, with the perimysium enveloping bundles of fibers (fascicles) and the covering the whole muscle. The term "endomysium" originates from roots "endo-" meaning within and "mys" meaning muscle, reflecting its position encircling individual fibers. While analogous thin connective tissue layers exist around fibers in smooth and cardiac muscle and are also termed endomysium, the structure is more pronounced and distinctly organized in skeletal muscle. These layers in non-skeletal muscles are often thinner and integrated with basal laminae, but they serve similar supportive roles.

Relationship to Other Connective Tissues

The endomysium forms the innermost layer of the intramuscular connective tissue hierarchy, enveloping individual skeletal muscle fibers, while the perimysium surrounds bundles of these fibers known as fascicles, and the epimysium encases the entire muscle belly. This nested arrangement creates a cohesive structural framework that integrates muscle fibers into functional units, with the endomysium providing immediate support to single fibers and progressively thicker layers organizing larger assemblages. Endomysial fibers interconnect seamlessly with the perimysium through periodic junction plates, forming a continuous three-dimensional lattice that extends throughout the muscle and merges with the at the periphery. This interconnected network anchors the muscle to tendons at its origins and insertions, ultimately linking to via the tendon-bone interface, thereby ensuring efficient force transmission from cellular to macroscopic scales. In terms of thickness, the endomysium is the thinnest layer at approximately 0.2–1.0 μm. The perimysium is intermediately thick and variable, while the is the thickest, with dimensions depending on muscle size. These relative dimensions reflect their roles in providing graduated mechanical reinforcement, with the delicate endomysium facilitating diffusion while denser outer layers offer broader protection. Variations in endomysial and perimysial thickness occur across muscle architectures, with pennate muscles exhibiting thicker layers to distribute forces from obliquely oriented fibers, whereas muscles have relatively thinner sheaths suited to their parallel fiber alignment and uniform contraction. Such adaptations optimize the for specific biomechanical demands, as seen in pennate muscles like the gastrocnemius where enhanced perimysial development supports greater force concentration.

Structure and Composition

Extracellular Matrix Components

The (ECM) of the endomysium primarily consists of fibers that provide structural integrity and tensile strength to individual muscle fibers. is the predominant isoform, forming thick fibrils that contribute to the overall stiffness and load-bearing capacity of the endomysium, while type III collagen assembles into finer reticular fibers that enhance flexibility and support the three-dimensional network around each myofiber. Type VI collagen is also present, forming microfibrils that connect the to the fibrillar ECM. is specifically enriched in the , the thin layer immediately surrounding the muscle fiber , where it forms a meshwork that anchors the ECM to the cell surface. Reticular fibers, composed mainly of type III collagen, interweave with these structures to create a delicate scaffold, and fibers are interspersed throughout, imparting elasticity to accommodate and relaxation without rupture. Glycoproteins and further modulate the ECM's biochemical properties, facilitating interactions between the matrix and muscle cells. and are key adhesion molecules that bind on the myofiber surface, promoting stable attachment and signaling for muscle maintenance, while , a small leucine-rich proteoglycan, regulates fibril assembly and provides hydration through its chains. Hyaluronan, a non-sulfated , is abundant in the endomysial space, where it forms a hydrated gel-like network that lubricates fiber sliding during contraction and buffers mechanical stress. The endomysial ECM integrates with the basement membrane to form a specialized dual-layer architecture. The inner basal lamina, rich in type IV collagen and laminin, fuses seamlessly with the outer reticular layer of the endomysium, creating a continuous barrier that isolates each muscle fiber while allowing nutrient diffusion. This integration ensures compartmentalization and protects against shear forces during muscle activity. Quantitatively, the endomysial ECM constitutes approximately 0.1–1.2% of skeletal muscle dry mass, with collagen content varying by muscle type—typically higher in postural muscles like the soleus (up to 8-10 mg/g tissue) compared to fast-twitch muscles like the gastrocnemius (around 4-6 mg/g), reflecting adaptations to chronic versus phasic loading.

Cellular Elements

The endomysium harbors a variety of resident cellular elements that interact with muscle fibers to maintain structural integrity, facilitate repair, and support physiological functions. These include fibroblasts, which serve as the primary producers of (ECM) proteins such as collagens, providing essential structural support to individual muscle fibers. Satellite cells function as muscle stem cells, positioned between the and the , enabling muscle growth and regeneration. Macrophages contribute to immune surveillance by monitoring the tissue microenvironment and responding to microlesions to preserve . Capillary endothelial cells line the vessels embedded within the endomysial interstices, ensuring delivery and oxygen supply tailored to muscle fiber demands. Satellite cells occupy a specialized niche within the endomysium, where the ECM components, including in the , interact with such as α7β1 on satellite cell surfaces to anchor the cells and transduce mechanical signals that sustain quiescence. This microenvironment prevents premature activation while allowing satellite cells to re-enter the upon stimuli like , promoting proliferation and differentiation through shifts in integrin-mediated and signaling. Fibroblasts exhibit a sparse distribution in the endomysium, comprising a small proportion of total muscle cells and typically spreading along the length of individual fibers over distances of approximately 100 μm. In contrast, satellite cells represent about 2–7% of myonuclei in healthy adult , with their density declining with age due to reduced regenerative capacity and increasing with such as exercise to enhance repair potential. These cellular elements engage in dynamic interactions that reinforce endomysial function. Fibroblasts respond to mechanical stress by upregulating ECM synthesis, including production driven by cytokines like TGF-β, to adapt the matrix stiffness and support force transmission. Macrophages, particularly resident subsets, perform immune surveillance by cloaking minor tissue damage to limit inflammation, and infiltrating macrophages clear necrotic debris post-injury through , facilitating timely resolution and preventing . The endomysial ECM serves as a scaffold that spatially organizes these cells around muscle fibers, enabling coordinated responses to physiological demands.

Function

Mechanical Roles

The endomysial collagen lattice, composed primarily of type I and III s, facilitates the distribution of contractile forces both laterally and longitudinally across muscle fibers. This occurs through shear interactions between adjacent fibers, where the collagen network realigns in response to muscle length changes, transmitting active force from myofibers to surrounding tissues and preventing localized or misalignment during contraction. Disruption of endomysial connections can reduce active force production by up to 22%, highlighting its essential role in maintaining efficient force transfer within fiber bundles. In terms of elasticity and compliance, the endomysium exhibits non-linear elastic properties, allowing significant stretch and to accommodate fiber shortening and lengthening during contraction. fibers within the endomysial enhance this compliance, enabling individual muscle fibers to slide relative to one another within fascicles while preserving overall bundle integrity. This viscoelastic behavior contributes to passive force generation, with endomysial disruption decreasing passive stress by approximately 26%, thereby altering the muscle's length-tension relationship. The endomysium also provides structural integrity by acting as a mechanical buffer, absorbing and dissipating shear stresses generated during dynamic muscle activity to protect fibers from damage. Its thin, continuous sheath (0.2–1.0 μm thick) links the to the broader via collagen IV and laminins, reducing localized shear and preventing fiber injury under load. Defects in this network, such as those from enzymatic degradation, lead to increased fiber vulnerability and diminished output. Biomechanically, the endomysium demonstrates tensile properties influenced by cross-linking density, with mature cross-links (e.g., pyridinoline) enhancing and strength compared to immature ones. Its ranges from 3.7–5 kPa, supporting compliant deformation under physiological strains, while integration with the perimysium allows coordinated whole-muscle force transmission. Overall tensile strength in endomysial-enriched muscle preparations approximates 0.2–0.5 MPa, with modulus varying based on maturity ratios of 2.6–6.6.

Vascular and Neural Support

The endomysium serves as a critical conduit for the vascular network essential to function, embedding a dense array of that run parallel to individual muscle . These endomysial form an interconnected microvascular bed surrounding each , facilitating the direct delivery of oxygen and nutrients while removing metabolic byproducts. In oxidative muscles, such as those in endurance-trained individuals, capillary typically ranges from 300 to 600 per mm², ensuring efficient tailored to high metabolic demands. Neural elements within the endomysium include motor nerve endings that form neuromuscular junctions, where terminals branch and penetrate the to directly with the muscle fiber . This anchoring stabilizes the junction, enabling precise transmission of action potentials for contraction. Additionally, endings embedded in the endomysium contribute to by detecting muscle stretch and tension, integrating with broader neural feedback mechanisms. Lymphatic drainage in the endomysium is mediated by fine lymphatic vessels originating near beds, which collect interstitial fluid and waste products for return to the systemic circulation. These vessels integrate closely with the vascular network, promoting efficient clearance during muscle activity. The areolar composition of the endomysium enhances its permeability, allowing gradients for metabolite exchange between vessels and muscle fibers, thereby supporting sustained demands without significant barriers.

Development and Physiology

Embryonic Development

Skeletal muscle fibers originate from the somitic mesoderm during embryonic development, while the endomysium forms as part of the connective tissue framework produced by fibroblasts derived from mesenchymal progenitors in the lateral plate mesoderm. This layer arises alongside the differentiation of paraxial mesoderm into somites, which give rise to the myogenic components of muscle. Endomysial fibroblasts derive from mesenchymal progenitors associated with the developing muscle, distinct from the myogenic lineage marked by Pax3 and Pax7 expression. In human fetuses, the endomysium is observable by week 12 of , forming a more defined network around individual muscle fibers, as observed in analyses of fetal hyoid muscle tissues. At earlier stages, fibroblast-like cells infiltrate the developing muscle primordia, initiating the deposition of components. The formation process involves fibroblasts migrating alongside myoblasts to ensheath nascent muscle fibers, first secreting components of the , such as and , followed by reticular fibers composed primarily of type III collagen. This sequential assembly is regulated by genes including Col1a1, which encodes essential for the structural integrity of the maturing endomysium. Developmental timelines vary across species, occurring more rapidly in ; in mice, endomysial extracellular matrix deposition starts around embryonic days 12-14, preceding full muscle-tendon integration. These processes are modulated by growth factors such as TGF-β, which influences differentiation and matrix production during early .

Role in Muscle Regeneration

Following muscle injury, the endomysium undergoes partial degradation mediated by matrix metalloproteinases (MMP-2 and MMP-9), which disrupts its collagen-rich structure and releases embedded growth factors such as (VEGF) and insulin-like growth factor-1 (IGF-1) to initiate repair signaling. This degradation creates a permissive environment within the endomysial niche, activating satellite cells—resident muscle stem cells—that proliferate and differentiate into myoblasts to fuse with damaged fibers. The endomysium's components, including collagen IV and , further support satellite cell adhesion and migration during this acute response. In the repair phase, endomysial fibroblasts become activated to remodel the (ECM), synthesizing and depositing new types I, III, and VI to restore structural integrity and provide a scaffold for myofiber regeneration. Concurrently, macrophages infiltrate the endomysium, transitioning from pro-inflammatory (M1) to () phenotypes to clear necrotic debris and secrete cytokines that promote myoblast differentiation and ECM reorganization. These cellular interactions, coordinated via endomysial signaling pathways like PI3K/Akt, ensure efficient tissue rebuilding without excessive scarring in acute injuries. During muscle adaptation, such as in response to or exercise, the endomysium thickens through increased deposition and ECM remodeling, enhancing its capacity for lateral force transmission between fibers and improving overall muscle compliance. Exercise-induced mechanical loading stimulates activity and MMP expression in the endomysium, allowing dynamic adjustments that support satellite cell expansion and fiber growth while maintaining ECM elasticity. This adaptive remodeling is evident in fibronectin-mediated pathways that regulate satellite cell function during repeated bouts of activity. However, in chronic injuries, overactive endomysial fibroblasts driven by transforming growth factor-beta (TGF-β) signaling can lead to excessive ECM deposition and , forming rigid that disrupts satellite cell niches and impairs functional regeneration. This fibrotic response reduces the endomysium's compliance, hindering force transmission and increasing susceptibility to re-injury.

Clinical Significance

Pathological Changes

In muscular dystrophies, particularly (DMD), the endomysium undergoes significant pathological thickening and due to the absence of , which normally stabilizes muscle fiber membranes. This deficiency results in membrane fragility, influx of calcium and sodium ions, cellular , and subsequent myofiber , triggering an inflammatory response that promotes excessive deposition within the endomysium. Unlike the thin, delicate normal endomysium that provides minimal structural support, the fibrotic endomysium in DMD replaces functional muscle tissue with scar-like connective tissue, exacerbating muscle weakness and limiting ambulation. Histological analysis reveals that endomysial correlates strongly with poor motor outcomes, such as reduced strength, and appears early in disease progression, often before widespread degeneration. Quantitative assessments via demonstrate a marked expansion of endomysial volume in DMD, with mean thickness increases ranging from 4- to 7-fold in areas of low and exceeding 15-fold in high- regions, reflecting the progressive replacement of muscle . This is driven by fibrogenic factors like transforming growth factor-beta (TGF-β), leading to accumulation and chronic tissue remodeling that impairs muscle contractility. In aging and , the endomysium exhibits stiffening primarily through increased cross-linking and advanced glycation end products (AGEs), which alter the composition and reduce its compliance compared to the more elastic structure in younger muscle. These changes, including heightened aggregation in the endomysial layer, contribute to diminished regenerative capacity by hindering satellite cell migration and differentiation, thereby accelerating . Sarcopenia, characterized by progressive loss of muscle mass and strength, becomes prevalent after age 60, affecting up to 10-50% of older adults depending on diagnostic criteria, with endomysial stiffening exacerbating functional decline. Inflammatory myopathies, such as , feature endomysial infiltration by immune cells that disrupt the structural integrity of this layer. Predominantly composed of + T lymphocytes and macrophages, these endomysial mononuclear infiltrates surround and invade non-necrotic muscle fibers, inducing cytotoxic damage and inflammation that compromises the endomysium's supportive role. This immune-mediated attack leads to focal disruptions in endomysial architecture, promoting further muscle fiber injury and impaired force transmission, distinct from the fibrotic dominance seen in dystrophies.

Diagnostic and Therapeutic Implications

Diagnostic assessment of the endomysium relies on advanced imaging and biopsy techniques to evaluate its ultrastructure and integrity, particularly in conditions involving such as muscular dystrophies (MD). Electron microscopy provides detailed visualization of the endomysial network, revealing its fine fibrous architecture composed of fibrils and components surrounding individual muscle fibers. This method is valuable for identifying ultrastructural disruptions in the endomysium, such as irregularities in fiber alignment or matrix density, which can inform diagnoses of neuromuscular disorders. (MRI), specifically T2 mapping, enables noninvasive quantification of by detecting alterations in T2 relaxation times correlated with content in the endomysium and surrounding . In fibrotic muscle, T2 mapping shows decreased relaxation times associated with increased endomysial deposition, offering a quantitative for disease progression. Muscle remains a for direct evaluation of endomysial composition, utilizing (IHC) to stain key proteins like IV and , which form the interface with muscle fibers. Abnormal staining patterns, such as reduced expression or thickened IV layers, indicate endomysial remodeling and are diagnostic for MD subtypes like . These IHC analyses help differentiate dystrophic changes from other myopathies by assessing the integrity of the endomysial barrier, which supports satellite cell function and muscle fiber stability. Therapeutic strategies targeting the endomysium focus on mitigating and restoring matrix to improve muscle function in models. Anti-fibrotic drugs like losartan, an , have demonstrated efficacy in reducing endomysial accumulation by inhibiting transforming growth factor-β signaling, leading to decreased and enhanced muscle regeneration in murine models. In LAMA2-related models, losartan treatment significantly ameliorated endomysial , preserving cell niches essential for repair. therapies aim to correct genetic defects that disrupt endomysial integrity, thereby stabilizing cell niches; for instance, dystrophin-restoring approaches in Duchenne models improve interactions and niche microenvironment for activation. Emerging research explores endomysial scaffolds for delivery to promote regeneration, leveraging the native matrix as a biocompatible platform. Decellularized endomysium-permeable hydrogels facilitate satellite cell engraftment and myogenic differentiation, enhancing muscle mass recovery in models without eliciting immune rejection. As of 2025, preclinical studies using these scaffolds show promise for clinical translation, with ongoing investigations into their integration with therapies to target fibrotic niches in MD. Recent 2025 preclinical studies have explored anti-fibrotic antibody-drug conjugates targeting lysyl oxidase (LOX) to inhibit cross-linking in endomysial , demonstrating reduced and improved muscle function in DMD models.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK537236/
  2. https://training.seer.cancer.gov/anatomy/muscular/structure.html
  3. https://pressbooks-dev.oer.hawaii.edu/anatomyandphysiology/chapter/skeletal-muscle/
  4. https://books.byui.edu/bio_461_principles_o/structural_organization
  5. https://books.byui.edu/bio_461_principles_o/structural_organizat
  6. https://www.ncbi.nlm.nih.gov/books/NBK537139/
  7. http://medsci.indiana.edu/histo/docs/glos.htm
  8. https://www.ncbi.nlm.nih.gov/books/NBK537195/
  9. https://courses.lumenlearning.com/suny-ap1/chapter/smooth-muscle/
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC3177172/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC7248366/
  12. https://doi.org/10.3389/fphys.2020.00495
  13. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.00495/full
  14. https://doi.org/10.1016/j.jsb.2007.01.022
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC5079803/
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC10635663/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC3325159/
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC9309511/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC7096581/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC4073943/
  21. https://www.sciencedirect.com/science/article/pii/S0021929025004695
  22. https://www.sciencedirect.com/science/article/pii/S0021929024002124
  23. https://www.sciencedirect.com/science/article/pii/S0021929020302529
  24. https://onlinelibrary.wiley.com/doi/10.1111/sms.14442
  25. https://journals.physiology.org/doi/full/10.1152/physiol.00026.2015
  26. https://www.ncbi.nlm.nih.gov/books/NBK57140/
  27. https://link.springer.com/content/pdf/10.1007/978-3-211-99390-3_156.pdf
  28. https://www.elsevier.com/resources/anatomy/skeletal-muscle-fiber/motor-nerve-fiber/motor-neuron/16106
  29. https://www.sciencedirect.com/topics/medicine-and-dentistry/endomysium
  30. https://www.worldscientific.com/doi/pdf/10.1142/9789813207158_0004
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC11267076/
  32. https://journals.biologists.com/dev/article/144/12/2104/48055/Making-muscle-skeletal-myogenesis-in-vivo-and-in
  33. https://www.nature.com/articles/s41536-022-00216-9
  34. https://pubmed.ncbi.nlm.nih.gov/9871403/
  35. https://www.researchgate.net/publication/19211817_Fibroblasts_promote_the_formation_of_a_continuous_basal_lamina_during_myogenesis_in_vitro
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC11038350/
  37. https://www.nature.com/articles/s42003-025-08653-0
  38. https://doi.org/10.1006/dbio.1998.9107
  39. https://doi.org/10.1016/j.stem.2012.09.015
  40. https://inflammregen.biomedcentral.com/articles/10.1186/s41232-023-00308-z
  41. https://doi.org/10.1096/fj.14-266668
  42. https://doi.org/10.1007/s00441-018-2955-2
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC5393925/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC3631802/
  45. https://academic.oup.com/jnen/article/68/7/762/2917096
  46. https://pubmed.ncbi.nlm.nih.gov/19535995/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC4024417/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC8614898/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC6223729/
  50. https://www.ncbi.nlm.nih.gov/books/NBK6196/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC1906803/
  52. https://journals.lww.com/ijpm/fulltext/2022/65001/electron_microscopy_in_the_diagnosis_of_skeletal.35.aspx
  53. https://www.nature.com/articles/s41598-020-78747-8
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC7496817/
  55. https://jamanetwork.com/journals/jamaneurology/fullarticle/579483
  56. https://www.sciencedirect.com/science/article/pii/S0960896614000029
  57. https://academic.oup.com/jnen/article/64/3/181/2916631
  58. https://pubmed.ncbi.nlm.nih.gov/22522482/
  59. https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2020.00003/full
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC6211823/
  61. https://www.sciencedirect.com/science/article/abs/pii/S1385894724013913
  62. https://www.liebertpub.com/doi/full/10.1089/wound.2024.0049?doi=10.1089/wound.2024.0049
  63. https://www.cell.com/iscience/fulltext/S2589-0042(25)00596-6
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