Mitochondrial Fission Inhibition is a targeted molecular strategy to pharmacologically or nutritionally restrain the excessive fragmentation of the mitochondrial network within a cell. Fission is a natural process, but chronic or unchecked division leads to smaller, dysfunctional mitochondria that are prone to oxidative stress and reduced ATP production, a hallmark of cellular aging. The clinical objective of inhibition is to promote mitochondrial fusion, thereby maintaining a healthy, interconnected, and functionally robust mitochondrial network.
Origin
This concept originates from the specialized field of mitochondrial dynamics, a sub-discipline of cellular biology that studies the continuous process of fusion and fission that shapes the mitochondrial network. Its relevance to hormonal health and longevity stems from the recognition that mitochondrial dysfunction is a central driver of metabolic and endocrine decline. The strategy is based on controlling the balance of key regulatory proteins like DRP1 and Mfn1/2.
Mechanism
Inhibition is achieved by directly or indirectly interfering with the activity of pro-fission proteins, such as Dynamin-related protein 1 (DRP1), which is responsible for constricting and dividing the mitochondrial membrane. By reducing DRP1 activity, the balance shifts toward fusion, a process mediated by Mitofusins (Mfn1 and Mfn2) and OPA1. This stabilization of the network facilitates the repair and quality control of mitochondria, sustaining high-efficiency cellular energy production.
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