Mitochondrial dysfunction and mitophagy: crucial players in burn trauma and wound healing

Prabhakaran, Harshini Sheeja; Hu, Dongxue; Wang, He; Luo, Gaoxing; Liou, Yih‐Cherng

doi:10.1093/burnst/tkad029

Cited by 7 publications

(2 citation statements)

References 180 publications

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“…Lastly, a 2023 review article detailed the correlation of burn injury progression with mitochondrial homeostasis, which is mediated via burn injury-induced hyperinflammation and subsequent mitochondrial dysfunction and cell death [ 50 ]. As mitophagy maintains cellular homeostasis by the selective removal of damaged mitochondria, the authors suggested that the process of mitophagy could be a promising therapeutic strategy for wound healing and burn injury.…”

Section: Mitochondria Dysfunction and Dermatological Manifestationsmentioning

confidence: 99%

“…As mitophagy maintains cellular homeostasis by the selective removal of damaged mitochondria, the authors suggested that the process of mitophagy could be a promising therapeutic strategy for wound healing and burn injury. Furthermore, the authors discuss Pink1 and Parkin activators and USP30 inhibitors as potential therapeutic agents for the regulation of mitophagy and the subsequent mitigation of burn injury progression [ 50 ].…”

Section: Mitochondria Dysfunction and Dermatological Manifestationsmentioning

confidence: 99%

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Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature

Natarelli,

Gahoonia,

Aflatooni

et al. 2024

IJMS

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Mitochondria are eukaryotic cellular organelles that function in energy metabolism, ROS production, and programmed cell death. Cutaneous epithelial and hair follicle dermal papilla cells are energy-rich cells that thereby may be affected by mitochondrial dysfunction and DNA mutation accumulation. In this review, we aimed to summarize the medical literature assessing dermatologic conditions and outcomes associated with mitochondrial dysfunction. A search of PubMed and Embase was performed with subsequent handsearching to retrieve additional relevant articles. Mitochondrial DNA (mtDNA) deletions, mutation accumulation, and damage are associated with phenotypic signs of cutaneous aging, hair loss, and impaired wound healing. In addition, several dermatologic conditions are associated with aberrant mitochondrial activity, such as systemic lupus erythematosus, psoriasis, vitiligo, and atopic dermatitis. Mouse model studies have better established causality between mitochondrial damage and dermatologic outcomes, with some depicting reversibility upon restoration of mitochondrial function. Mitochondrial function mediates a variety of dermatologic conditions, and mitochondrial components may be a promising target for therapeutic strategies.

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Section: Mitochondria Dysfunction and Dermatological Manifestationsmentioning

confidence: 99%

Section: Mitochondria Dysfunction and Dermatological Manifestationsmentioning

confidence: 99%

Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature

Natarelli,

Gahoonia,

Aflatooni

et al. 2024

IJMS

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Lubricin‐Inspired Nanozymes Reconstruct Cartilage Lubrication System with an “In‐Out” Strategy

Du,

Chen,

Liu

et al. 2024

Small Methods

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Lubricin, secreted primarily by chondrocytes, plays a critical role in maintaining the function of the cartilage lubrication system. However, both external factors such as friction and internal factors like oxidative stress can disrupt this system, leading to osteoarthritis. Inspired by lubricin, a lubricating nanozyme, that is, Poly‐2‐acrylamide‐2‐methylpropanesulfonic acid sodium salt‐grafted aminofullerene, is developed to restore the cartilage lubrication system using an “In‐Out” strategy. The “Out” aspect involves reducing friction through a combination of hydration lubrication and ball‐bearing lubrication. Simultaneously, the “In” aspect aims to mitigate oxidative stress by reducing free radical, increasing autophagy, and improving the mitochondrial respiratory chain. This results in reduced chondrocyte senescence and increased lubricin production, enhancing the natural lubrication ability of cartilage. Transcriptome sequencing and Western blot results demonstrate that it enhances the functionality of mitochondrial respiratory chain complexes I, III, and V, thereby improving mitochondrial function in chondrocytes. In vitro and in vivo experiments show that the lubricating nanozymes reduce cartilage wear, improve chondrocyte senescence, and mitigate oxidative stress damage, thereby mitigating the progression of osteoarthritis. These findings provide novel insights into treating diseases associated with oxidative stress and frictional damage, such as osteoarthritis, and set the stage for future research and development of therapeutic interventions.

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Therapeutic effect of mitochondrial transplantation on burn injury

Li,

Cao,

Liu

et al. 2024

Free Radical Biology and Medicine

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Mitochondrial dysfunction and mitophagy: crucial players in burn trauma and wound healing

Cited by 7 publications

References 180 publications

Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature

Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature

Lubricin‐Inspired Nanozymes Reconstruct Cartilage Lubrication System with an “In‐Out” Strategy

Therapeutic effect of mitochondrial transplantation on burn injury

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