P47 Investigating the influence of aged-related basement membrane Laminin-332 loss in mitochondrial function
Clicks: 2
ID: 318459
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
0.3
/100
2 views
1 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #227 of 304 articles by views in the british journal of dermatology
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 304 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
Abstract Introduction and aims Mitochondrial function is increasingly implicated in healthy epidermal homeostasis. From energy production, regulation of apoptosis and metabolism, to reactive oxygen species (ROS) and calcium signalling. This organelle plays a critical role in ensuring the integrity of the skin barrier by regulating proliferation and differentiation of basal keratinocytes. The integrity of this barrier is essential in protection against pathogenic entry, ultraviolet (UV) radiation and transepidermal water loss. Owing to their multifaceted role, mitochondria are one of the interdependent hallmark alterations associated with the process of ageing. In ageing skin, mitochondria are observed to have increased ROS levels, while simultaneously showing a decrease in both turnover and adenosine triphosphate production. A key alteration associated with skin ageing is the gradual reduction of essential skin basement membrane proteins, such as Laminin 332. Analysis of RNA-sequencing data highlighted that mitochondrial pathways were downregulated with the loss of laminin α-3 chain of Laminin 332. Methods Characterization of these altered mitochondrial pathways was conducted in laminin α-3 chain knockdown immortalized keratinocytes (sHLAMA3). Mitochondria in laminin knockdown cell display abnormal distribution and morphology. Results Functional assays suggest this mitochondrial altered morphology is a consequence of impaired mitochondrial quality, dynamics and mitophagy signalling pathways. An imbalance in mitochondrial fission and fusion has been identified as a potential consequence of impaired downstream integrin and focal adhesion signalling. Conclusions Our findings indicate that Laminin 332 loss profoundly impacts mitochondrial organization and function. Understanding the interplay between basement membrane components and mitochondrial dynamics offers new insight into skin ageing and highlights potential therapeutic targets to restore barrier function and cellular homeostasis.
| Reference Key |
openalex_W7165623269
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Leonor Ferreira Lopes |
| Journal | the british journal of dermatology |
| Year | 2026 |
| DOI |
10.1093/bjd/ljag151.086
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.