PMID- 37506377
OWN - NLM
STAT- MEDLINE
DCOM- 20231023
LR  - 20231024
IS  - 1533-4023 (Electronic)
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 82
IP  - 4
DP  - 2023 Oct 1
TI  - San Jie Tong Mai Fang Protects Against Atherosclerosis Progression by Regulating 
      Macroautophagy through the PI3K/AKT/mTOR Signaling Pathway.
PG  - 333-343
LID - 10.1097/FJC.0000000000001452 [doi]
AB  - Many studies have confirmed that macrophage autophagy injury negatively impacts 
      the pathogenesis of atherosclerosis (AS). Meanwhile, the phosphoinositide 
      3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) 
      signaling pathway affects AS progression by regulating macrophage autophagy. We 
      previously reported that the herbal formula San Jie Tong Mai Fang (SJTMF) elicits 
      lipid regulatory and anti-inflammatory properties. Hence, the current study used 
      an ApoE -/- high-fat diet-fed mouse model to determine whether SJTMF elicits 
      protective effects against AS progression by means of the regulation of 
      macrophage autophagy through the PI3K/AKT/mTOR signaling pathway. Our results 
      show that SJTMF reduced the number of atherosclerotic plaques, foam cell 
      formation, and intimal thickness in mouse aorta. In addition, SJTMF improved 
      blood lipid metabolism and inflammatory levels in mice. We also observed that 
      SJTMF caused macrophages to be polarized toward the M2 phenotype through the 
      inhibition of the PI3K/AKT/mTOR signaling pathway. In addition, the abundances of 
      LC3-II/I and beclin1 proteins-key autophagy molecules-were increased, whereas 
      that of p62 was decreased, resulting in the promotion of macrophage autophagy. 
      Taken together, these findings indicate that SJTMF may regulate the polarization 
      of macrophages by inhibiting the PI3K/AKT/mTOR signaling pathway, thereby 
      reducing atherosclerotic plaque damage in ApoE -/- mice, thereby promoting 
      macrophage autophagy and eliciting a significant antiarteriosclerosis effect. 
      Hence, SJTMF may represent a promising new candidate drug for the treatment of 
      AS.
CI  - Copyright (c) 2023 The Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Li, Pengfei
AU  - Li P
AUID- ORCID: 0000-0002-7864-3538
AD  - College of Traditional Chinese Medicine, Changchun University of Chinese 
      Medicine, Changchun, 130117, People's of Republic of China.
FAU - Li, Hongyu
AU  - Li H
AD  - Department of Cardiology, the Third Affiliated Hospital of Changchun University 
      of Chinese Medicine, Changchun, People's of Republic of China.
FAU - Li, Xiaohui
AU  - Li X
AD  - Department of Cardiology, the First Affiliated Hospital of Henan University of 
      Chinese Medicine, Zhengzhou, People's of Republic of China.
FAU - Li, Shuangdi
AU  - Li S
AD  - Department of Cardiology, the Affiliated Hospital of Changchun University of 
      Chinese Medicine, Changchun, People's of Republic of China.
FAU - Xu, Hanying
AU  - Xu H
AD  - College of Traditional Chinese Medicine, Changchun University of Chinese 
      Medicine, Changchun, 130117, People's of Republic of China.
FAU - Cui, Junfeng
AU  - Cui J
AD  - Office of the Party Committee, the Affiliated Hospital of Changchun University of 
      Chinese Medicine, Changchun, People's of Republic of China.
FAU - Cheng, Guangyu
AU  - Cheng G
AD  - Research Center of Traditional Chinese Medicine, the Affiliated Hospital of 
      Changchun University of Chinese Medicine, Changchun 130117, People's of Republic 
      of China; and.
FAU - Liu, Yinghui
AU  - Liu Y
AD  - Department of Basic Teaching and Research of Traditional Chinese Medicine, 
      Changchun University of Chinese Medicine, Changchun, People's of Republic of 
      China.
FAU - Xu, Xiaolin
AU  - Xu X
AD  - Department of Cardiology, the Affiliated Hospital of Changchun University of 
      Chinese Medicine, Changchun, People's of Republic of China.
FAU - Xin, Yuning
AU  - Xin Y
AD  - College of Traditional Chinese Medicine, Changchun University of Chinese 
      Medicine, Changchun, 130117, People's of Republic of China.
FAU - Liu, Aidong
AU  - Liu A
AD  - Department of Cardiology, the Third Affiliated Hospital of Changchun University 
      of Chinese Medicine, Changchun, People's of Republic of China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20231001
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Apolipoproteins E)
SB  - IM
MH  - Mice
MH  - Animals
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphatidylinositol 3-Kinase/metabolism
MH  - Macroautophagy
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Mice, Knockout, ApoE
MH  - Signal Transduction
MH  - *Atherosclerosis/drug therapy/prevention & control/genetics
MH  - *Plaque, Atherosclerotic
MH  - Autophagy
MH  - Apolipoproteins E/pharmacology
MH  - Mammals/metabolism
PMC - PMC10545065
COIS- The authors report no conflicts of interest.
EDAT- 2023/07/28 19:11
MHDA- 2023/10/23 12:45
PMCR- 2023/10/02
CRDT- 2023/07/28 16:52
PHST- 2022/10/29 00:00 [received]
PHST- 2023/06/30 00:00 [accepted]
PHST- 2023/10/23 12:45 [medline]
PHST- 2023/07/28 19:11 [pubmed]
PHST- 2023/07/28 16:52 [entrez]
PHST- 2023/10/02 00:00 [pmc-release]
AID - 00005344-990000000-00205 [pii]
AID - JCVP-22-662 [pii]
AID - 10.1097/FJC.0000000000001452 [doi]
PST - epublish
SO  - J Cardiovasc Pharmacol. 2023 Oct 1;82(4):333-343. doi: 
      10.1097/FJC.0000000000001452.