PMID- 30422673
OWN - NLM
STAT- MEDLINE
DCOM- 20191104
LR  - 20200225
IS  - 1205-7541 (Electronic)
IS  - 0008-4212 (Print)
IS  - 0008-4212 (Linking)
VI  - 97
IP  - 6
DP  - 2019 Jun
TI  - Restoration of skeletal muscle homeostasis by hydrogen sulfide during 
      hyperhomocysteinemia-mediated oxidative/ER stress condition (1).
PG  - 441-456
LID - 10.1139/cjpp-2018-0501 [doi]
AB  - Elevated homocysteine (Hcy), i.e., hyperhomocysteinemia (HHcy), causes skeletal 
      muscle myopathy. Among many cellular and metabolic alterations caused by HHcy, 
      oxidative and endoplasmic reticulum (ER) stress are considered the major ones; 
      however, the precise molecular mechanism(s) in this process is unclear. 
      Nevertheless, there is no treatment option available to treat HHcy-mediated 
      muscle injury. Hydrogen sulfide (H(2)S) is increasingly recognized as a potent 
      anti-oxidant, anti-apoptotic/necrotic/pyroptotic, and anti-inflammatory compound 
      and also has been shown to improve angiogenesis during ischemic injury. Patients 
      with CBS mutation produce less H(2)S, making them vulnerable to Hcy-mediated 
      cellular damage. Many studies have reported bidirectional regulation of ER stress 
      in apoptosis through JNK activation and concomitant attenuation of cell 
      proliferation and protein synthesis via PI3K/AKT axis. Whether H(2)S mitigates 
      these detrimental effects of HHcy on muscle remains unexplored. In this review, 
      we discuss molecular mechanisms of HHcy-mediated oxidative/ER stress responses, 
      apoptosis, angiogenesis, and atrophic changes in skeletal muscle and how H(2)S 
      can restore skeletal muscle homeostasis during HHcy condition. This review also 
      highlights the molecular mechanisms on how H(2)S could be developed as a 
      clinically relevant therapeutic option for chronic conditions that are aggravated 
      by HHcy.
FAU - Majumder, Avisek
AU  - Majumder A
AD  - a Department of Physiology, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
AD  - b Biochemistry and Molecular Genetics, University of Louisville School of 
      Medicine, Louisville, KY 40202, USA.
FAU - Singh, Mahavir
AU  - Singh M
AD  - a Department of Physiology, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
AD  - c Eye and Vision Science Laboratory, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
FAU - George, Akash K
AU  - George AK
AD  - a Department of Physiology, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
AD  - c Eye and Vision Science Laboratory, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
FAU - Tyagi, Suresh C
AU  - Tyagi SC
AD  - a Department of Physiology, University of Louisville School of Medicine, 
      Louisville, KY 40202, USA.
LA  - eng
GR  - R01 AR071789/AR/NIAMS NIH HHS/United States
GR  - R01 HL107640/HL/NHLBI NIH HHS/United States
GR  - R01 NS084823/NS/NINDS NIH HHS/United States
GR  - U01 HL074815/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20181113
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - *Endoplasmic Reticulum Stress
MH  - *Homeostasis
MH  - Humans
MH  - Hydrogen Sulfide/*metabolism
MH  - Hyperhomocysteinemia/*metabolism/pathology
MH  - Muscle, Skeletal/*metabolism/pathology
MH  - *Oxidative Stress
PMC - PMC6719301
MID - NIHMS1048083
OTO - NOTNLM
OT  - JNK
OT  - angiogenesis
OT  - angiogenese
OT  - apoptose
OT  - apoptosis
OT  - atrophie
OT  - atrophy
OT  - cystathionine-beta synthase
OT  - desequilibre redox (derives reactifs de l'oxygene)
OT  - endoplasmic reticulum stress
OT  - inflammation
OT  - ischemia
OT  - ischemie
OT  - myopathie
OT  - myopathy
OT  - redox imbalance (ROS)
OT  - stress du reticulum endoplasmique
COIS- Conflict of interest The authors declare that there is no conflict of interest 
      associated with this work.
EDAT- 2018/11/14 06:00
MHDA- 2019/11/05 06:00
PMCR- 2019/09/03
CRDT- 2018/11/14 06:00
PHST- 2018/11/14 06:00 [pubmed]
PHST- 2019/11/05 06:00 [medline]
PHST- 2018/11/14 06:00 [entrez]
PHST- 2019/09/03 00:00 [pmc-release]
AID - 10.1139/cjpp-2018-0501 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2019 Jun;97(6):441-456. doi: 10.1139/cjpp-2018-0501. 
      Epub 2018 Nov 13.