Autophagy, tissue repair, and fibrosis: a delicate balance

Migneault, Francis; Hébert, Marie‐Josée

doi:10.1016/j.matbio.2021.01.003

Cited by 45 publications

(31 citation statements)

References 131 publications

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“…On THP-1 macrophages, for instance, the endocytosis of archaeolipids is suggested to induce autophagy [ 73 ]. Physiological levels of autophagy are key for a correct wound healing and epithelial repair of the alveoli [ 74 ]. The reparation of the ALI model induced by nebulized nATC thus may be related to the establishment of synergy between archaeolipids and CUR.…”

Section: Discussionmentioning

confidence: 99%

Reparation of an Inflamed Air-Liquid Interface Cultured A549 Cells with Nebulized Nanocurcumin

et al. 2021

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The anti-inflammatory, antifibrotic and antimicrobial activities of curcumin (CUR) are missed because of its low solubility in aqueous media, low bioavailability, and structural lability upon oral intake. Soft nanoparticles such as nanoliposomes are not efficient as CUR carriers, since crystalline CUR is expelled from them to physiological media. Nanostructures to efficiently trap and increase the aqueous solubility of CUR are needed to improve both oral or nebulized delivery of CUR. Here we showed that SRA1 targeted nanoarchaeosomes (nATC) [1:0.4 w:w:0.04] archaeolipids, tween 80 and CUR, 155 ± 16 nm sized of −20.7 ± 3.3 z potential, retained 0.22 mg CUR ± 0.09 per 12.9 mg lipids ± 4.0 (~600 μM CUR) in front to dilution, storage, and nebulization. Raman and fluorescence spectra and SAXS patterns were compatible with a mixture of enol and keto CUR tautomers trapped within the depths of nATC bilayer. Between 20 and 5 µg CUR/mL, nATC was endocytosed by THP1 and A549 liquid–liquid monolayers without noticeable cytotoxicity. Five micrograms of CUR/mL nATC nebulized on an inflamed air–liquid interface of A549 cells increased TEER, normalized the permeation of LY, and decreased il6, tnfα, and il8 levels. Overall, these results suggest the modified pharmacodynamics of CUR in nATC is useful for epithelia repair upon inflammatory damage, deserving further deeper exploration, particularly related to its targeting ability.

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Section: Discussionmentioning

confidence: 99%

Reparation of an Inflamed Air-Liquid Interface Cultured A549 Cells with Nebulized Nanocurcumin

et al. 2021

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“…Emerging evidence suggests that autophagy can play a central role in the maintenance of homeostasis in wide variety of tissues [ 81 ]. Metabolites produced through autophagic activity, such as carbohydrates, amino acids, nucleosides, and fatty acids, are often essential for maintenance of tissue homeostasis.…”

Section: Relevance Of Autophagy To Human Diseasesmentioning

confidence: 99%

Targeting autophagy in disease: established and new strategies

et al. 2021

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Macroautophagy/autophagy is an evolutionarily conserved pathway responsible for clearing cytosolic aggregated proteins, damaged organelles or invading microorganisms. Dysfunctional autophagy leads to pathological accumulation of the cargo, which has been linked to a range of human diseases, including neurodegenerative diseases, infectious and autoimmune diseases and various forms of cancer. Cumulative work in animal models, application of genetic tools and pharmacologically active compounds, has suggested the potential therapeutic value of autophagy modulation in disease, as diverse as Huntington, Salmonella infection, or pancreatic cancer. Autophagy activation versus inhibition strategies are being explored, while the role of autophagy in pathophysiology is being studied in parallel. However, the progress of preclinical and clinical development of autophagy modulators has been greatly hampered by the paucity of selective pharmacological agents and biomarkers to dissect their precise impact on various forms of autophagy and cellular responses. Here, we summarize established and new strategies in autophagy-related drug discovery and indicate a path toward establishing a more efficient discovery of autophagy-selective pharmacological agents. With this knowledge at hand, modern concepts for therapeutic exploitation of autophagy might become more plausible.

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“…Additionally, remifentanil is a common, short-acting, synthetic opioid analgesic drug that inhibits oxidative stress-induced apoptosis of skin fibroblasts by activating autophagy [ 60 ]. Moreover, numerous studies have shown that autophagy activation and inhibition are closely related to fibroblast differentiation [ 61 ]. For example, observation of spatiotemporal changes in LC3-positive dots in fibroblasts and myofibroblasts in a rat model of wound healing revealed substantial increases in the number of LC3-positive dots during the late proliferative phase.…”

Section: Reviewmentioning

confidence: 99%

Autophagy and skin wound healing

et al. 2022

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Autophagy is a lysosome-dependent, self-renewal mechanism that can degrade and recycle cellular components in eukaryotic cells to maintain the stability of the intracellular environment and the cells ability to cope with unfavorable environments. Numerous studies suggest that autophagy participates in regulating various cellular functions and is closely associated with the onset and progression of various diseases. Wound healing is a complex, multistep biological process that involves multiple cell types. Refractory wounds, which include diabetic skin ulcers, can seriously endanger human health. Previous studies have confirmed that autophagy plays an essential role in various phases of wound healing. Specifically, in the inflammatory phase, autophagy has an anti-infection effect and it negatively regulates the inflammatory response, which prevents excessive inflammation from causing tissue damage. In the proliferative phase, local hypoxia in the wound can induce autophagy, which plays a role in anti-apoptosis and anti-oxidative stress and promotes cell survival. Autophagy of vascular endothelial cells promotes wound angiogenesis and that of keratinocytes promotes their differentiation, proliferation and migration, which is conducive to the completion of wound re-epithelialisation. In the remodeling phase, autophagy of fibroblasts affects the formation of hypertrophic scars. Additionally, a refractory diabetic wound may be associated with increased levels of autophagy, and the regulation of mesenchymal stem cell autophagy may improve its application to wound healing. Therefore, understanding the relationship between autophagy and skin wound healing and exploring the molecular mechanism of autophagy regulation may provide novel strategies for the clinical treatment of wound healing.

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Autophagy, tissue repair, and fibrosis: a delicate balance

Cited by 45 publications

References 131 publications

Reparation of an Inflamed Air-Liquid Interface Cultured A549 Cells with Nebulized Nanocurcumin

Reparation of an Inflamed Air-Liquid Interface Cultured A549 Cells with Nebulized Nanocurcumin

Targeting autophagy in disease: established and new strategies

Autophagy and skin wound healing

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