Cellular organelles have their own critical functions. For example, mitochondria are a power source to maintain cellular and tissue energy demand. However, recent expansion of pharmacological, molecular and genetic tools have allowed us to observe that these organelles have active intracellular as well as extracellular communications important for cell and organ homoeostasis. Disruption, chronic activation or de-compensation of such communication has been associated with a variety of pathophysiological conditions such as those seen in metabolic diseases, cardiovascular diseases and cancer. Several recent articles have demonstrated that pharmacological as well as genetic intervention to alter specific organelle communication/signal transduction could be useful to prevent pathology in experimental models of human diseases [1–3].
Recent publications in Clinical Science and other journals have contributed to research on organelle communication [4,5]. One example is a mitochondrial retro-grade or forward grade signal in response to stress that...
