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Author Notes:
Matthew B. Hudson, Renal Division, Department of Medicine, Emory University, Rm 3327 WMB, 1639 Pierce Dr. NE, Atlanta, GA 30322, Phone: (404) 727-3424, Fax: (404) 727-3425, mbhudso@emory.edu.
The authors have no conflicts of interest.
Subjects:
Research Funding:
Our work has been supported by grants from the National Institute of Diabetes, Digestive and Kidney Disease (RO1 DK-95610, S.R.P.) (T32 DK007656, M.B.H); the American Heart Association (GRNT7660020, S.R.P.); and the Department of Veterans Affairs (I01 BX001456, S.R.P.).
Keywords:
- Science & Technology
- Life Sciences & Biomedicine
- Biochemistry & Molecular Biology
- Cell Biology
- Calcineurin
- Skeletal muscle
- Atrophy
- Hypertrophy
- Cell signaling
- SKELETAL-MUSCLE
- GENE-EXPRESSION
- CARDIAC-HYPERTROPHY
- OXIDATIVE STRESS
- PGC-1-ALPHA EXPRESSION
- PROTEIN-DEGRADATION
- ATROPHY INVOLVE
- SOLEUS MUSCLE
- FIBER-TYPE
- UBIQUITIN
Calcineurin: A poorly understood regulator of muscle mass
Abstract:
This review will discuss the existing literature that has examined the role of calcineurin (CnA) in the regulation of skeletal muscle mass in conditions associated with hypertrophic growth or atrophy. Muscle mass is determined by the balance between protein synthesis and degradation which is controlled by a number of intracellular signaling pathways, most notably the insulin/IGF/phosphatidylinositol 3-kinase (PI3K)/Akt system. Despite being activated by IGF-1 and having well-described functions in the determination of muscle fiber phenotypes, calcineurin (CnA), a Ca2+-activated serine/threonine phosphatase, and its downstream signaling partners have garnered little attention as a regulator of muscle mass. Compared to other signaling pathways, the relatively few studies that have examined the role of CnA in the regulation of muscle size have produced discordant results. The reasons for these differences is not obvious but may be due to the selective nature of the genetic models studied, fluctuations in the endogenous level of CnA activity in various muscles, and the variable use of CnA inhibitors to inhibit CnA signaling. Despite the inconsistent nature of the outcomes, there is sufficient direct and indirect evidence to conclude that CnA plays a role in the regulation of skeletal muscle mass. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
Copyright information:
© 2013 Published by Elsevier Ltd.
This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).
