Seminar in Biological Mechanisms of Aging and Cancer/Mitochondrial Dysfunction

Mitochondria are cellular organelles which house the mechanics to produce most of the energy (ATP) made in the body. They achieve this high yield of ATP through the electron transport chain, ending with a ATP synthase, which makes ATP. In aging, mitochondrial dysfunction occurs when the efficiency of the machinery to make ATP, the electron transport chain, is decreased, leading to less production of ATP. Another contribution to mitochondrial dysfunction is oxidative stress, when the number of harmful reactive oxidative species is much greater than the body’s ability to remove them.

Mitochondrial dysfunction has had great evidence supporting its role in aging and research behind the mechanism of influence and how to repair this dysfunction have been in abundance in recent years. An example of research looking to repair mitochondrial dysfunction can be found in a paper we analyzed, which was published in 2010 by Brian Onken and Monica Driscoll [1]. These researchers were interested in how the mitochondrial dysfunction could be repaired by using the drug class, biguanides. Using C. elegans, they studied the biguanide drug, metformin, and how it influences the healthspan of the animals. In general, they found that metformin extends the median healthspan of the C. elegans, when components AMPK (AMP- protein kinase), LKB1 (threonine kinase) and SKN-1 transcription factor are present and active. When SKN-1 is active in the intestine, like when metformin is used, it leads to oxidative stress resistance, which is an attempt to repair mitochondrial dysfunction.

Below is our attempt to create a graphical abstract summarizing this paper.


  1. 1.0 1.1 Template:Onken, B. & Driscoll, M. (2010). Metformin Induces a Dietary Restriction-Like State and the Oxidative Stress Response to Entend ''C. elegans'' Healthspan via AMPK, LKB1, and SKN-1. PLoS ONE, 5(1), 1-13