PMID- 34966735
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211231
IS  - 2296-634X (Print)
IS  - 2296-634X (Electronic)
IS  - 2296-634X (Linking)
VI  - 9
DP  - 2021
TI  - ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure 
      Development During Chronic Catecholamine Stress.
PG  - 732952
LID - 10.3389/fcell.2021.732952 [doi]
LID - 732952
AB  - Heart failure development is characterized by persistent inflammation and 
      progressive fibrosis owing to chronic catecholamine stress. In a chronic stress 
      state, elevated catecholamines result in the overstimulation of beta-adrenergic 
      receptors (betaARs), specifically beta2-AR coupling with Galphai protein. Galphai signaling 
      increases the activation of receptor-stimulated p38 
      mitogen-activated-protein-kinases (p38 MAPKs) and extracellular signal-regulated 
      kinases (ERKs). Phosphorylation by these kinases is a common way to positively 
      regulate the catalytic activity of A Disintegrin and Metalloprotease 17 (ADAM17), 
      a metalloprotease that has grown much attention in recent years and has emerged 
      as a chief regulatory hub in inflammation, fibrosis, and immunity due to its 
      vital proteolytic activity. ADAM17 cleaves and activates proinflammatory 
      cytokines and fibrotic factors that enhance cardiac dysfunction via inflammation 
      and fibrosis. However, there is limited information on the cardiovascular aspect 
      of ADAM17, especially in heart failure. Hence, this concise review provides a 
      comprehensive insight into the structure of ADAM17, how it is activated and 
      regulated during chronic catecholamine stress in heart failure development. This 
      review highlights the inflammatory and fibrotic roles of ADAM17's substrates; 
      Tumor Necrosis Factor alpha (TNFalpha), soluble interleukin-6 receptor (sIL-6R), and 
      amphiregulin (AREG). Finally, how ADAM17-induced chronic inflammation and 
      progressive fibrosis aggravate cardiac dysfunction is discussed.
CI  - Copyright (c) 2021 Adu-Amankwaah, Adzika, Adekunle, Ndzie Noah, Mprah, Bushi, 
      Akhter, Huang, Xu, Adzraku, Nadeem and Sun.
FAU - Adu-Amankwaah, Joseph
AU  - Adu-Amankwaah J
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Adzika, Gabriel Komla
AU  - Adzika GK
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Adekunle, Adebayo Oluwafemi
AU  - Adekunle AO
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Ndzie Noah, Marie Louise
AU  - Ndzie Noah ML
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Mprah, Richard
AU  - Mprah R
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Bushi, Aisha
AU  - Bushi A
AD  - Xuzhou Medical University, Xuzhou, China.
FAU - Akhter, Nazma
AU  - Akhter N
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Huang, Fei
AU  - Huang F
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Xu, Yaxin
AU  - Xu Y
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
FAU - Adzraku, Seyram Yao
AU  - Adzraku SY
AD  - Key Laboratory of Bone Marrow Stem Cell, Department of Hematology, The Affiliated 
      Hospital of Xuzhou Medical University, Xuzhou, China.
FAU - Nadeem, Iqra
AU  - Nadeem I
AD  - Department of Neurobiology and Anatomy, Xuzhou Medical University, Xuzhou, China.
FAU - Sun, Hong
AU  - Sun H
AD  - Department of Physiology, Xuzhou Medical University, Xuzhou, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20211213
PL  - Switzerland
TA  - Front Cell Dev Biol
JT  - Frontiers in cell and developmental biology
JID - 101630250
PMC - PMC8710811
OTO - NOTNLM
OT  - ADAM17
OT  - cardiac fibrosis
OT  - cardiac inflammation
OT  - fibrotic factors
OT  - heart failure
OT  - metalloenzymes
OT  - pro-inflammatory cytokines
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/12/31 06:00
MHDA- 2021/12/31 06:01
PMCR- 2021/01/01
CRDT- 2021/12/30 05:42
PHST- 2021/06/29 00:00 [received]
PHST- 2021/11/16 00:00 [accepted]
PHST- 2021/12/30 05:42 [entrez]
PHST- 2021/12/31 06:00 [pubmed]
PHST- 2021/12/31 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 732952 [pii]
AID - 10.3389/fcell.2021.732952 [doi]
PST - epublish
SO  - Front Cell Dev Biol. 2021 Dec 13;9:732952. doi: 10.3389/fcell.2021.732952. 
      eCollection 2021.