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Biochemical Insight into Skin Regeneration and Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 October 2024) | Viewed by 3708

Special Issue Editor

Centre for Regenerative Medicine ‘‘Stefano Ferrari’’, University of Modena and Reggio Emilia, 41125 Modena, Italy
Interests: single-cell sequencing approaches; epidermal stem cells; biochemical signaling; DNA repair

Special Issue Information

Dear Colleagues,

Skin regeneration and inflammation are intricately linked processes with significant biochemical implications. The skin serves as a formidable barrier against external threats, and when damaged, it must swiftly and efficiently repair itself to maintain its integrity. This complex regenerative mechanism is orchestrated by a network of biochemical signals.

Inflammation plays a pivotal role in this process. When the skin is injured, immune cells and cytokines are recruited to the site of damage. These mediators stimulate cell proliferation, collagen synthesis, and angiogenesis, which are all essential for proper tissue repair. The biochemical cues involved are numerous, including growth factors and eventually shifts in the metabolic state.

Understanding the intricate balance of biochemical signals that modulate skin regeneration will improve the development of therapies that optimize the regenerative response while mitigating excessive inflammation.

The aim of this Special Issue is to summarize and enlarge the knowledge of the biochemical processes involved in skin regeneration in both homeostatic and inflammatory conditions.

Therefore, authors are invited to submit original research and review articles which address the progress and current standing of biochemical processes.

Topics of interest include, but are not limited to, the following:

  • Identification of new aspects of biochemical pathways involved in epithelial cells self-renewal and differentiation;
  • Identification of new aspects of biochemical pathways involved in fibroblasts/keratinocytes communication in epithelial regeneration and inflammation;
  • Techniques for the analysis and identification of biochemical pathways and networks;
  • Transcriptomic, epitranscriptomics, or proteomic analysis of skin regeneration and inflammation.

Dr. Elena Enzo
Guest Editor

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Keywords

  • skin regeneration
  • inflammation
  • extracellular matrix in wound healing
  • cell proliferation
  • self-renewal and differentiation

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Published Papers (1 paper)

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Research

17 pages, 5018 KiB  
Article
Poly-D,L-Lactic Acid Filler Attenuates Ultraviolet B-Induced Skin Pigmentation by Reducing Destruction of the Basement Membrane
by Kyung-A Byun, Suk Bae Seo, Seyeon Oh, Jong-Won Jang, Kuk Hui Son and Kyunghee Byun
Int. J. Mol. Sci. 2024, 25(21), 11568; https://doi.org/10.3390/ijms252111568 - 28 Oct 2024
Viewed by 3071
Abstract
Poly-D,L-lactic acid (PDLLA) filler, which increases volume and collagen synthesis, is used for skin rejuvenation. PDLLA filler also increases M2 macrophages and IL-10. Ultraviolet (UV) radiation induces dermal hyperpigmentation by disrupting the basement membrane (BM), allowing melanin to move into the dermis. Therefore, [...] Read more.
Poly-D,L-lactic acid (PDLLA) filler, which increases volume and collagen synthesis, is used for skin rejuvenation. PDLLA filler also increases M2 macrophages and IL-10. Ultraviolet (UV) radiation induces dermal hyperpigmentation by disrupting the basement membrane (BM), allowing melanin to move into the dermis. Therefore, using UV-irradiated macrophages and animal skin, we determined whether PDLLA filler decreased M1 macrophages and skin inflammation, thereby reducing BM destruction and dermal hyperpigmentation. UV radiation increased the M1 macrophage marker CD86 and TNF-α expression, which was inhibited by the treatment of macrophages with PDLLA. In fibroblasts treated with conditioned medium from UV-irradiated macrophages, NF-κB activity, NLRP3 inflammasome components (NLRP3, ASC, and pro-caspase-1), IL-18, MMP2, and MMP9 increased, but all decreased after PDLLA treatment. Similar to the in vitro study, UV-irradiated mouse skin showed increased CD86, NLRP3, ASC, pro-caspase-1, MMP2, and MMP9, which decreased after PDLLA injection. Disruption of the lamina densa of the BM and dermal pigmentation increased after UV irradiation and decreased after PDLLA injection. In conclusion, PDLLA reduced dermal pigmentation by decreasing BM destruction in UV-irradiated skin. PDLLA has the potential to reduce dermal pigmentation by regenerating the BM. Full article
(This article belongs to the Special Issue Biochemical Insight into Skin Regeneration and Inflammation)
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