PMID- 36597355
OWN - NLM
STAT- MEDLINE
DCOM- 20230321
LR  - 20230322
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Linking)
VI  - 38
IP  - 7-9
DP  - 2023 Mar
TI  - Nuclear Factor Erythroid 2-Related Factor 2 and Its Targets in Skeletal Muscle 
      Repair and Regeneration.
PG  - 619-642
LID - 10.1089/ars.2022.0208 [doi]
AB  - Significance: Skeletal muscles have a robust regenerative capacity in response to 
      acute and chronic injuries. Muscle repair and redox homeostasis are intimately 
      linked; increased generation of reactive oxygen species leads to cellular 
      dysfunction and contributes to muscle wasting and progression of muscle diseases. 
      In exemplary muscle disease, Duchenne muscular dystrophy (DMD), caused by 
      mutations in the DMD gene that encodes the muscle structural protein dystrophin, 
      the regeneration machinery is severely compromised, while oxidative stress 
      contributes to the progression of the disease. The nuclear factor erythroid 
      2-related factor 2 (NRF2) and its target genes, including heme oxygenase-1 
      (HO-1), provide protective mechanisms against oxidative insults. Recent Advances: 
      Relevant advances have been evolving in recent years in understanding the 
      mechanisms by which NRF2 regulates processes that contribute to effective muscle 
      regeneration. To this end, pathways related to muscle satellite cell 
      differentiation, oxidative stress, mitochondrial metabolism, inflammation, 
      fibrosis, and angiogenesis have been studied. The regulatory role of NRF2 in 
      skeletal muscle ferroptosis has been also suggested. Animal studies have shown 
      that NRF2 pathway activation can stop or reverse skeletal muscle pathology, 
      especially when endogenous stress defence mechanisms are imbalanced. Critical 
      Issues: Despite the growing recognition of NRF2 as a factor that regulates 
      various aspects of muscle regeneration, the mechanistic impact on muscle 
      pathology in various models of muscle injury remains imprecise. Future 
      Directions: Further studies are necessary to fully uncover the role of NRF2 in 
      muscle regeneration, both in physiological and pathological conditions, and to 
      investigate the possibilities for development of new therapeutic modalities. 
      Antioxid. Redox Signal. 38, 619-642.
FAU - Loboda, Agnieszka
AU  - Loboda A
AUID- ORCID: 0000-0003-3523-3560
AD  - Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and 
      Biotechnology, Jagiellonian University in Krakow, Krakow, Poland.
FAU - Dulak, Jozef
AU  - Dulak J
AD  - Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and 
      Biotechnology, Jagiellonian University in Krakow, Krakow, Poland.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20230302
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (NF-E2-Related Factor 2)
SB  - IM
MH  - Animals
MH  - *NF-E2-Related Factor 2/genetics/metabolism
MH  - Signal Transduction/physiology
MH  - Muscle, Skeletal/metabolism
MH  - *Muscular Dystrophy, Duchenne/genetics/pathology
MH  - Regeneration/physiology
OTO - NOTNLM
OT  - Duchenne muscular dystrophy
OT  - NRF2
OT  - heme oxygenase-1
OT  - microRNAs
OT  - muscle regeneration
OT  - oxidative stress
EDAT- 2023/01/05 06:00
MHDA- 2023/03/22 06:00
CRDT- 2023/01/04 01:33
PHST- 2023/01/05 06:00 [pubmed]
PHST- 2023/03/22 06:00 [medline]
PHST- 2023/01/04 01:33 [entrez]
AID - 10.1089/ars.2022.0208 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2023 Mar;38(7-9):619-642. doi: 10.1089/ars.2022.0208. Epub 
      2023 Mar 2.