As an essential organelle in nucleated eukaryotic cells, mitochondria play a central role in energy metabolism, maintenance of redox balance, and regulation of apoptosis. Mitochondrial dysfunction, either due to the TCA cycle enzyme defects, mitochondrial DNA genetic mutations, defective mitochondrial electron transport chain, oxidative stress, or aberrant oncogene and tumor suppressor signaling, has been observed in a wide spectrum of human cancers. In this review, we summarize mitochondrial dysfunction induced by these alterations that promote human cancers.

Following injury, tissue autonomously initiates a complex repair process, resulting in either partial recovery or regeneration of tissue architecture and function in most organisms. Both the repair and regeneration processes are highly coordinated by a hierarchy of interplay among signal transduction pathways initiated by different growth factors, cytokines and other signaling molecules under normal conditions. However, under chronic traumatic or pathological conditions, the reparative or regenerative process of most tissues in different organs can lose control to different extents, leading to random, incomplete or even flawed cell and tissue reconstitution and thus often partial restoration of the original structure and function, accompanied by the development of fibrosis, scarring or even pathogenesis that could cause organ failure and death of the organism. Ample evidence suggests that the various combinatorial fibroblast growth factor (FGF) and receptor signal transduction systems play prominent roles in injury repair and the remodeling of adult tissues in addition to embryonic development and regulation of metabolic homeostasis. In this review, we attempt to provide a brief update on our current understanding of the roles, the underlying mechanisms and clinical application of FGFs in tissue injury repair.