Contact Between Mitochondrion and Endoplasmic Reticulum in the Context of Aging
Mitochondria are the power plants of the cell, generating chemical energy store molecules to power cellular operations. The endoplasmic reticulum is a structure studded with ribosomes for protein assembly, and where protein folding and transport within the cell takes place. Nothing in the cell has only one function, however, and both of these structures influence many cell processes. Researchers here discuss what is known of the direct interactions that take place between mitochondrion and endoplasmic reticulum, and the possible relevance of this still largely unexplored activity to aging and disease.
For decades, scientists viewed the various compartments within cells, called organelles, as relatively independent entities. This perspective, while useful for understanding basic cellular structure, has proven to be an oversimplification of the complex and dynamic nature of cellular organization. Recent research has revealed a far more interconnected and fluid cellular landscape, where organelles interact and communicate in sophisticated ways.
At the heart of this paradigm shift is the discovery of specialized regions where two critical organelles - mitochondria and the endoplasmic reticulum (ER) - are in close apposition. These regions, known as mitochondria-associated ER membranes (MAMs), are revolutionizing our understanding of cellular function and disease. MAMs act as cellular 'communication hubs', allowing for rapid and precise exchange of signals and molecules between mitochondria and the ER. This communication is crucial for maintaining cellular health, responding to stress and regulating energy production. The strategic positioning of MAMs allows for efficient transfer of molecules and signals, facilitating precise control of cellular functions.
Alterations in MAM structure and function have been implicated in a wide range of conditions, including neurodegenerative diseases, metabolic disorders, and cardiovascular disease. Disruption of MAMs impairs the structural and functional connectivity between the ER and mitochondria, leading to significant cellular dysfunction. For instance, studies have shown that high glucose levels can disrupt MAM integrity through the pentose phosphate pathway, resulting in mitochondrial fragmentation and altered respiration. While some age-related changes in MAMs have been observed, such as alterations in calcium signalling and mitochondrial function, the full impact of these changes on cellular function and organismal health remains an open question. Understanding how MAMs change throughout the lifespan could provide insights into the ageing process and potentially lead to interventions to promote healthy ageing.