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REV-ERB and ROR: therapeutic targets for treating myopathies.

Abstract Muscle is primarily known for its mechanical roles in locomotion, maintenance of posture, and regulation of cardiac and respiratory function. There are numerous medical conditions that adversely affect muscle, myopathies that disrupt muscle development, regeneration and protein turnover to detrimental effect. Skeletal muscle is also a vital secretory organ that regulates thermogenesis, inflammatory signaling and directs context specific global metabolic changes in energy substrate preference on a daily basis. Myopathies differ in the causative factors that drive them but share common features including severe reduction in quality of life and significantly increased mortality all due irrefutably to the loss of muscle mass. Thus far clinically viable approaches for preserving muscle proteins and stimulating new muscle growth without unwanted side effects or limited efficacy has been elusive. Over the last few decades, evidence has emerged through in vitro and in vivo studies that suggest the nuclear receptors REV-ERB and ROR might modulate pathways involved in myogenesis and mitochondrial biogenesis. Hinting that REV-ERB and ROR might be targeted to treat myopathies. However there is still a need for substantial investigation into the roles of these nuclear receptors in in vivo rodent models of degenerative muscle diseases and acute injury. Although exciting, REV-ERB and ROR have somewhat confounding roles in muscle physiology and therefore more studies utilizing in vivo models of skeletal muscle myopathies are needed. In this review we highlight the molecular forces driving some of the major degenerative muscular diseases and showcase two promising molecular targets that may have the potential to treat myopathies: ROR and REV-ERB.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title physical biology
Publication Year Start




PMID- 28586319
OWN - NLM
STAT- In-Process
DA  - 20170606
LR  - 20170606
IS  - 1478-3975 (Electronic)
IS  - 1478-3967 (Linking)
VI  - 14
IP  - 4
DP  - 2017 Jun 06
TI  - REV-ERB and ROR: therapeutic targets for treating myopathies.
PG  - 045002
LID - 10.1088/1478-3975/14/4/045002 [doi]
AB  - Muscle is primarily known for its mechanical roles in locomotion, maintenance of 
      posture, and regulation of cardiac and respiratory function. There are numerous
      medical conditions that adversely affect muscle, myopathies that disrupt muscle
      development, regeneration and protein turnover to detrimental effect. Skeletal
      muscle is also a vital secretory organ that regulates thermogenesis, inflammatory
      signaling and directs context specific global metabolic changes in energy
      substrate preference on a daily basis. Myopathies differ in the causative factors
      that drive them but share common features including severe reduction in quality
      of life and significantly increased mortality all due irrefutably to the loss of 
      muscle mass. Thus far clinically viable approaches for preserving muscle proteins
      and stimulating new muscle growth without unwanted side effects or limited
      efficacy has been elusive. Over the last few decades, evidence has emerged
      through in vitro and in vivo studies that suggest the nuclear receptors REV-ERB
      and ROR might modulate pathways involved in myogenesis and mitochondrial
      biogenesis. Hinting that REV-ERB and ROR might be targeted to treat myopathies.
      However there is still a need for substantial investigation into the roles of
      these nuclear receptors in in vivo rodent models of degenerative muscle diseases 
      and acute injury. Although exciting, REV-ERB and ROR have somewhat confounding
      roles in muscle physiology and therefore more studies utilizing in vivo models of
      skeletal muscle myopathies are needed. In this review we highlight the molecular 
      forces driving some of the major degenerative muscular diseases and showcase two 
      promising molecular targets that may have the potential to treat myopathies: ROR 
      and REV-ERB.
FAU - Welch, Ryan D
AU  - Welch RD
AD  - Department of Pharmacology and Physiology, Saint Louis University School of
      Medicine, Saint Louis, MO, United States of America.
FAU - Flaveny, Colin A
AU  - Flaveny CA
LA  - eng
PT  - Journal Article
DEP - 20170606
PL  - England
TA  - Phys Biol
JT  - Physical biology
JID - 101197454
EDAT- 2017/06/07 06:00
MHDA- 2017/06/07 06:00
CRDT- 2017/06/07 06:00
AID - 10.1088/1478-3975/14/4/045002 [doi]
PST - epublish
SO  - Phys Biol. 2017 Jun 6;14(4):045002. doi: 10.1088/1478-3975/14/4/045002.

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