Do We Age Because We Have Mitochondria?

This is the question posed and not answered by a recent paper from a German institution, accompanied by a very tersely worded abstract: Do we age because we have mitochondria? The process of aging remains a great riddle. Production of reactive oxygen species (ROS) by mitochondria is an inevitable by-product of respiration, which has led to a hypothesis proposing the oxidative impairment of mitochondrial components (e.g., mtDNA, proteins, lipids) that initiates a vicious cycle of dysfunctional respiratory complexes producing more ROS, which again impairs function. This does not exclude other processes acting in parallel or targets for ROS action in other organelles than mitochondria. Given that aging is defined as the process leading to death, the role of mitochondria-based impairments in those organ systems responsible for human death (e.g., the cardiovascular system, cerebral dysfunction, and cancer) is described within the context of "garbage" accumulation and increasing insulin resistance, type 2 diabetes, and glycation of proteins. The processes involved in mitochondria-based impairments are very similar across a large range of organisms. Therefore, studies on model organisms from yeast, fungi, nematodes, flies to vertebrates, and from cells to organisms also add considerably to the understanding of human aging. Would we age without mitochondria? Certainly. Mitochondrial damage and dysfunction is only one of the most likely fundamental differences between young tis...
Source: Fight Aging! - Category: Health Medicine and Bioethics Commentators Authors: Tags: Medicine, Biotech, Research Source Type: blogs