The clinical history of both type-1 (T1D) and type-2 (T2D) diabetes differs drastically; however, the resultant conditions and complications often overlap. A common feature of both TD1 and TD2 is the failure to preserve muscle mass and function, here designated as diabetic myopathy. This complication, which is often overlooked, is believed to contribute to the progression of diabetic complications because the key role skeletal muscle plays in glucose homeostasis and locomotion. Despite the wealth of information on muscle weakness and muscle wasting, the specific triggering events of diabetic myopathy in people with diabetes remain unknown. Unfortunately, this condition currently also receives little attention in the clinical setting.

Several studies have investigated the link between diabetic myopathy and diverse cellular processes; however, further knowledge of the pathophysiological and molecular mechanisms involved in the onset and progression of diabetic myopathy is needed for the development of new pharmacological tools to ameliorate diabetic myopathy. New studies in the field of muscle biomedical research will propel novel insights to further our understanding of diabetic myopathy.

In this special issue of the Journal of Diabetes Research entitle “The Underlying Mechanisms of Diabetic Myopathy,” we call for original and review articles from leading and emerging scientists who study diabetic myopathy in different muscle tissues (cardiac, smooth, or skeletal) and with diverse expertise and interests, aiming to stimulate the continuing effort to understand the impact of diabetes on muscle function. In vitro and in vivo studies using diabetes animal models as well as interventional and/or translational studies are welcome. A wide array of topics and approaches on skeletal muscle pathophysiology in diabetes research are covered.

Potential topics include but are not limited to the following:

• Cellular studies (sarcolemma and T-tubules architecture, filament assembly, microtubules, regulation of cross-bridges formation, force generation, oxidative stress, Ca2+ signaling, intracellular pathways, proliferation, cellular fusion, regeneration, inflammation, serum factors, cytokines, adipokines, and myokines)
• Organ studies (histology, contractility and metabolic studies, and muscle lipid metabolism and its crosstalk with the nervous, circulatory, digestive, hepatic, and adipose tissues)
• Animal studies in vivo (e.g., muscle performance and exercise, obesity, aging, and statin-induced myopathy in diabetic patients or in animal models of diabetes)