This review summarizes our current understanding of how defective insulin signaling impacts cardiac function in diabetic cardiomyopathy and discusses the potential role of mitochondrial dynamics.
Specifically, better understanding of the defective or hyperactive signalling pathways in cancer cells has been the major focus of mechanistic studies of cancer progression and differentiation, as well as in the identification of candidate markers for diagnosis and therapeutic targets (Petricoin et al, 2005).
Or is something more subtle at play (defective trafficking?)? Reviewer #1: Clear mechanistic understanding of the VEGF signaling pathway is of paramount importance since this pathway lies in the heart of vascular biology and is being targeted to treat a number of human diseases.
Thus, for an in-depth understanding of defect engineering, clearly, theoretical methods are needed as an additional tool to predict the relative stability of potential defective structures and to support the interpretation of spectroscopic results.
Analysis of other seedling plastid-defective mutants should provide a better understanding of plastid formation during this critical period in plant development.
But our understanding of the mechanisms involved remains defective, perhaps because there is no way of relating the many different, and often proxy, measures of socio-economic status: social standing lacks the definitude of death.
In order to improve our understanding of such faulty responses and consequently develop efficient therapeutic strategies against the related diseases it is important to identify the molecular components encompassing normal and defective mechanotransduction.
Hence, deeper understanding of the molecular mechanisms of apoptosis and its defective status opens the gate for a new class of targeted therapeutics.
As a consequence of the lack of suitable characterization methods and developed analytical procedures, a molecular-level understanding of the electronic and steric properties at the defective sites is limited.
Defective mitochondrial translation is a major cause of mitochondrial disorders and proper understanding of its mechanisms and consequences is fundamental to rational treatment design.
