PMID- 34244974
OWN - NLM
STAT- MEDLINE
DCOM- 20220203
LR  - 20220203
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 476
IP  - 11
DP  - 2021 Nov
TI  - Role of PI3K/Akt signaling pathway in cardiac fibrosis.
PG  - 4045-4059
LID - 10.1007/s11010-021-04219-w [doi]
AB  - Heart failure (HF) is considered as a severe health problem worldwide, while 
      cardiac fibrosis is one of the main driving factors for the progress of HF. 
      Cardiac fibrosis was characterized by changes in cardiomyocytes, cardiac 
      fibroblasts, ratio of collagen (COL) I/III, and the excessive production and 
      deposition of extracellular matrix (ECM), thus forming a scar tissue, which leads 
      to pathological process of cardiac structural changes and systolic as well as 
      diastolic dysfunction. Cardiac fibrosis is a common pathological change of many 
      advanced cardiovascular diseases including ischemic heart disease, hypertension, 
      and HF. Accumulated studies have proven that phosphoinositol-3 kinase (PI3K)/Akt 
      signaling pathway is involved in regulating the occurrence, progression and 
      pathological formation of cardiac fibrosis via regulating cell survival, 
      apoptosis, growth, cardiac contractility and even the transcription of related 
      genes through a series of molecules including mammalian target of rapamycin 
      (mTOR), glycogen synthase kinase 3 (GSK-3), forkhead box proteins O1/3 (FoxO1/3), 
      and nitric oxide synthase (NOS). Thus, the review focuses on the role of PI3K/Akt 
      signaling pathway in the cardiac fibrosis. The information reviewed here should 
      be significant in understanding the role of PI3K/Akt in cardiac fibrosis and 
      contribute to the design of further studies related to PI3K/Akt and the cardiac 
      fibrotic response, as well as sought to shed light on a potential treatment for 
      cardiac fibrosis.
CI  - (c) 2021. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Qin, Wuming
AU  - Qin W
AD  - College of Life Sciences, Hunan Normal University, Changsha, 410006, Hunan, 
      China.
FAU - Cao, Linghui
AU  - Cao L
AUID- ORCID: 0000-0002-9203-2477
AD  - Changsha Central Hospital, Changsha, 410004, Hunan, China. 
      caolinghui1989@126.com.
FAU - Massey, Isaac Yaw
AU  - Massey IY
AD  - Department of Occupational and Environmental Health, Xiangya School of Public 
      Health Central South University, Changsha, 410078, Hunan, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210710
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Fibrosis/metabolism/pathology
MH  - Heart Diseases/*metabolism/*pathology
MH  - Humans
MH  - Myocardium/*metabolism/*pathology
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Cardiac fibrosis
OT  - PI3K/Akt signaling pathway
EDAT- 2021/07/11 06:00
MHDA- 2022/02/04 06:00
CRDT- 2021/07/10 06:27
PHST- 2021/03/09 00:00 [received]
PHST- 2021/06/29 00:00 [accepted]
PHST- 2021/07/11 06:00 [pubmed]
PHST- 2022/02/04 06:00 [medline]
PHST- 2021/07/10 06:27 [entrez]
AID - 10.1007/s11010-021-04219-w [pii]
AID - 10.1007/s11010-021-04219-w [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2021 Nov;476(11):4045-4059. doi: 10.1007/s11010-021-04219-w. 
      Epub 2021 Jul 10.