New insights into balancing wound healing and scarless skin repair

Journal of Tissue Engineering, Год журнала: 2023, Номер 14

Опубликована: Янв. 1, 2023

Scars caused by skin injuries after burns, wounds, abrasions and operations have serious physical psychological effects on patients. In recent years, the research of scar free wound repair has been greatly expanded. However, understanding complex mechanisms healing, in which various cells, cytokines mechanical force interact, is critical to developing a treatment that can achieve scarless healing. Therefore, this paper reviews types mechanism formation healing process, current progress dual consideration prevention, some strategies for repair.

Язык: Английский

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TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis

Aging and Disease, Год журнала: 2023, Номер 14(5), С. 1633 - 1633

Опубликована: Янв. 1, 2023

Fibrosis is the abnormal accumulation of extracellular matrix proteins such as collagen and fibronectin. Aging, injury, infections, inflammation can cause different types tissue fibrosis. Numerous clinical investigations have shown a correlation between degree liver pulmonary fibrosis in patients telomere length mitochondrial DNA content, both which are signs aging. Aging involves gradual loss function over time, results homeostasis and, ultimately, an organism's fitness. A major feature aging senescent cells. Senescent cells abnormally continuously accumulate late stages life, contributing to age-related deterioration, among other characteristics. Furthermore, generates chronic inflammation, decreases organ function. This finding suggests that closely related. The transforming growth factor-beta (TGF-β) superfamily plays crucial role physiological pathological processes aging, immune regulation, atherosclerosis, In this review, functions TGF-β normal organs, fibrotic tissues discussed: signalling altered with age indicator pathology associated addition, review discusses potential targeting noncoding.

Язык: Английский

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Sfrp1 inhibits lung fibroblast invasion during transition to injury-induced myofibroblasts

European Respiratory Journal, Год журнала: 2024, Номер 63(2), С. 2301326 - 2301326

Опубликована: Янв. 11, 2024

Fibroblast-to-myofibroblast conversion is a major driver of tissue remodelling in organ fibrosis. Distinct lineages fibroblasts support homeostatic niche functions, yet their specific activation states and phenotypic trajectories during injury repair have remained unclear.

Язык: Английский

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Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities

Circulation Research, Год журнала: 2024, Номер 134(12), С. 1718 - 1751

Опубликована: Июнь 6, 2024

The adult mammalian heart has limited endogenous regenerative capacity and heals through the activation of inflammatory fibrogenic cascades that ultimately result in formation a scar. After infarction, massive cardiomyocyte death releases broad range damage-associated molecular patterns initiate both myocardial systemic responses. TLRs (toll-like receptors) NLRs (NOD-like recognize (DAMPs) transduce downstream proinflammatory signals, leading to upregulation cytokines (such as interleukin-1, TNF-α [tumor necrosis factor-α], interleukin-6) chemokines CCL2 [CC chemokine ligand 2]) recruitment neutrophils, monocytes, lymphocytes. Expansion diversification cardiac macrophages infarcted play major role clearance infarct from dead cells subsequent stimulation reparative pathways. Efferocytosis triggers induction release anti-inflammatory mediators restrain reaction set stage for fibroblasts vascular cells. Growth factor–mediated pathways, neurohumoral cascades, matricellular proteins deposited provisional matrix stimulate fibroblast proliferation myofibroblast conversion. Deposition well-organized collagen-based extracellular network protects catastrophic rupture attenuates ventricular dilation. Scar maturation requires signals inhibit activity prevent excessive fibrosis. Moreover, mature scar, neovessels acquire mural cell coat contributes stabilization microvascular network. Excessive, prolonged, or dysregulated accentuate adverse remodeling dysfunction. leukocytes can contribute arrhythmogenesis. Inflammatory pathways may be promising therapeutic targets attenuate failure progression arrhythmia generation patients surviving infarction.

Язык: Английский

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Exosome/antimicrobial peptide laden hydrogel wound dressings promote scarless wound healing through miR-21-5p-mediated multiple functions

Biomaterials, Год журнала: 2024, Номер 308, С. 122558 - 122558

Опубликована: Апрель 2, 2024

Язык: Английский

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