Organ Crosstalk Contributes to Muscle Wasting in Chronic Kidney Disease

Abstract

Muscle wasting (ie, atrophy) is a serious consequence of chronic kidney disease (CKD) that reduces muscle strength and function. It reduces the quality of life for CKD patients and increases the risks of comorbidities and mortality. Current treatment strategies to prevent or reverse skeletal muscle loss are limited owing to the broad and systemic nature of the initiating signals and the multifaceted catabolic mechanisms that accelerate muscle protein degradation and impair protein synthesis and repair pathways. Recent evidence has shown how organs such as muscle, adipose, and kidney communicate with each other through interorgan exchange of proteins and RNAs during CKD. This crosstalk changes cell functions in the recipient organs and represents an added dimension in the complex processes that are responsible for muscle atrophy in CKD. This complexity creates challenges for the development of effective therapies to ameliorate muscle wasting and weakness in patients with CKD.