PMID- 32069832
OWN - NLM
STAT- MEDLINE
DCOM- 20210316
LR  - 20210316
IS  - 2218-273X (Electronic)
IS  - 2218-273X (Linking)
VI  - 10
IP  - 2
DP  - 2020 Feb 13
TI  - Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and 
      Clinical Implications.
LID - 10.3390/biom10020291 [doi]
LID - 291
AB  - Obesity is characterized by the excessive deposition of fat that may interfere 
      with the normal metabolic process of the body. It is a chronic condition 
      associated with various metabolic syndromes, whose prevalence is grossly 
      increasing, and affects both children and adults. Accumulation of excessive 
      macronutrients on the adipose tissues promotes the secretion and release of 
      inflammatory mediators, including interleukin-6 (IL-6), interleukin 1beta, tumor 
      necrotic factor-alpha (TNF-alpha), leptin, and stimulation of monocyte chemoattractant 
      protein-1 (MCP-1), which subsequently reduce the production of adiponectin 
      thereby initiating a proinflammatory state. During obesity, adipose tissue 
      synthesizes and releases a large number of hormones and cytokines that alter the 
      metabolic processes, with a profound influence on endothelial dysfunction, a 
      situation associated with the formation of atherosclerotic plaque. Endothelial 
      cells respond to inflammation and stimulation of MCP-1, which is described as the 
      activation of adhesion molecules leading to proliferation and transmigration of 
      leukocytes, which facilitates their increase in atherogenic and thromboembolic 
      potentials. Endothelial dysfunction forms the cornerstone of this discussion, as 
      it has been considered as the initiator in the progression of cardiovascular 
      diseases in obesity. Overexpression of proinflammatory cytokines with subsequent 
      reduction of anti-inflammatory markers in obesity, is considered to be the link 
      between obesity-induced inflammation and endothelial dysfunction. Inhibition of 
      inflammatory mechanisms and management and control of obesity can assist in 
      reducing the risks associated with cardiovascular complications.
FAU - Kwaifa, Ibrahim Kalle
AU  - Kwaifa IK
AD  - Department of Pathology, Faculty of Medicine and Health Sciences, Universiti 
      Putra Malaysia (UPM), Selangor 43400, Malaysia.
AD  - Department of Haematology, School of Medical Laboratory Sciences, College of 
      Health Sciences, Usmanu Danfodiyo University (UDU), Sokoto, North-Western 2346, 
      Nigeria.
FAU - Bahari, Hasnah
AU  - Bahari H
AD  - Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti 
      Putra Malaysia (UPM), Selangor 43400, Malaysia.
FAU - Yong, Yoke Keong
AU  - Yong YK
AD  - Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti 
      Putra Malaysia (UPM), Selangor 43400, Malaysia.
FAU - Noor, Sabariah Md
AU  - Noor SM
AUID- ORCID: 0000-0002-2292-5149
AD  - Department of Pathology, Faculty of Medicine and Health Sciences, Universiti 
      Putra Malaysia (UPM), Selangor 43400, Malaysia.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200213
PL  - Switzerland
TA  - Biomolecules
JT  - Biomolecules
JID - 101596414
RN  - 0 (Adiponectin)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adiponectin
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents
MH  - Atherosclerosis/metabolism
MH  - Chemokine CCL2/metabolism
MH  - Cytokines/metabolism
MH  - Endothelial Cells/*metabolism/pathology
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Insulin Resistance/physiology
MH  - Interleukin-6/metabolism
MH  - Metabolic Syndrome/pathology
MH  - Obesity/complications/*immunology
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC7072669
OTO - NOTNLM
OT  - adipose tissue
OT  - atherosclerosis
OT  - endothelial dysfunction
OT  - inflammation
OT  - obesity
COIS- The authors declared no conflict of interest.
EDAT- 2020/02/20 06:00
MHDA- 2021/03/17 06:00
PMCR- 2020/02/01
CRDT- 2020/02/20 06:00
PHST- 2019/08/27 00:00 [received]
PHST- 2019/10/04 00:00 [revised]
PHST- 2019/10/05 00:00 [accepted]
PHST- 2020/02/20 06:00 [entrez]
PHST- 2020/02/20 06:00 [pubmed]
PHST- 2021/03/17 06:00 [medline]
PHST- 2020/02/01 00:00 [pmc-release]
AID - biom10020291 [pii]
AID - biomolecules-10-00291 [pii]
AID - 10.3390/biom10020291 [doi]
PST - epublish
SO  - Biomolecules. 2020 Feb 13;10(2):291. doi: 10.3390/biom10020291.