It is a great pleasure to welcome Ms. Ines Martic, Universität Innsbruck, Austria, at Skin Ageing & Challenges 2024 this November in Malta. 

Topic: Mitophagy and Extracellular Vesicles: Mechanisms of Mitochondrial Quality Control in Skin Aging.

Presentation Highlights

• Mitophagy and Skin Aging: UVB-induced cellular stress in skin fibroblasts impairs mitochondrial function, triggering NIX-dependent mitophagy as a crucial mechanism for maintaining mitochondrial quality during aging.
• Extracellular Vesicles and Mitochondrial Clearance: In NIX-depleted fibroblasts, UVB irradiation leads to impaired mitophagy. This is compensated by the release of mitochondria-enriched extracellular vesicles, suggesting an alternative pathway for mitochondrial quality control.
• Implications for Aging and Skin Health: Understanding the interplay between mitophagy, extracellular vesicles, and mitochondrial health can uncover novel therapeutic targets for skin aging and cellular homeostasis

What is NIX?

NIX, also known as BNIP3L (BCL2 Interacting Protein 3-Like), is a mitochondrial protein crucial for mitophagy, which is the selective degradation of damaged or dysfunctional mitochondria. NIX is part of the BCL-2 family of proteins that regulate cell survival and death, particularly apoptosis. During cellular stress (e.g., hypoxia or oxidative stress), NIX recruits autophagosomes to engulf and degrade damaged mitochondria.

In addition to mitophagy, NIX plays a role in mitochondrial fission, allowing the segregation of damaged mitochondria. In summary, NIX is upregulated under stress conditions and works to preserve mitochondrial quality control. In some cases, NIX can also induce apoptosis by altering mitochondrial membrane potential. This makes NIX especially important in aged cells, where mitochondrial dysfunction is a hallmark of senescence and age-related diseases.