Abstract:Coronary heart disease (CHD) has been associated with significant morbidity and mortality worldwide. Although remain controversial, several studies have demonstrated the association of M. pneumoniae infections with atherosclerosis. We evaluated the possible association of mycoplasma infections in patients diagnosed with atherosclerosis by ELISA and PCR methods. Atherosclerotic tissue samples and blood samples were collected for the detection of mycoplasma antibodies (IgA) by ELISA from the 97 patients with cor… Show more
“…HDL, a key lipoprotein in the blood, can remove excess cholesterol from arterial walls and transport it back to the liver to be metabolized and eliminated, thus protecting the cardiovascular system ( 68 , 69 ). M. pneumoniae infection is associated with decreased HDL levels by enhancing the inflammatory response and disrupting lipid metabolism, which promote cholesterol deposition in the arterial wall and increase risk of atherosclerosis and cardiovascular disease ( 9 ). However, the association between M. pneumoniae infection and HDL levels is not clear due to differences in study sample size, study design and clinical characteristics of the disease; other influencing factors between infection and HDL levels need to be further explored.…”
Section: Association Between M Pneumoniae Infection and Hdl Metabolismmentioning
confidence: 99%
“…In addition, these infections show seasonal epidemics, usually peaking in winter and early spring (7). M. pneumoniae infection can change the blood lipid content of patients and accelerate occurrence and development of cardiovascular diseases such as coronary heart disease and atherosclerosis (8)(9)(10).…”
The association between
Mycoplasma pneumoniae
(
M. pneumoniae
) infection, high-density lipoprotein metabolism and cardiovascular disease is an emerging research area. The present review summarizes the basic characteristics of
M. pneumoniae
infection and its association with high-density lipoprotein and cardiovascular health.
M. pneumoniae
primarily invades the respiratory tract and damages the cardiovascular system through various mechanisms including adhesion, invasion, secretion of metabolites, production of autoantibodies and stimulation of cytokine production. Additionally, the present review highlights the potential role of high-density lipoprotein for the development of prevention and intervention of
M. pneumoniae
infection and cardiovascular disease, and provides suggestions for future research directions and clinical practice. It is urgent to explore the specific mechanisms underlying the association between
M. pneumoniae
infection, high-density lipoprotein metabolism, and cardiovascular disease and analyze the roles of the immune system and inflammatory response.
“…HDL, a key lipoprotein in the blood, can remove excess cholesterol from arterial walls and transport it back to the liver to be metabolized and eliminated, thus protecting the cardiovascular system ( 68 , 69 ). M. pneumoniae infection is associated with decreased HDL levels by enhancing the inflammatory response and disrupting lipid metabolism, which promote cholesterol deposition in the arterial wall and increase risk of atherosclerosis and cardiovascular disease ( 9 ). However, the association between M. pneumoniae infection and HDL levels is not clear due to differences in study sample size, study design and clinical characteristics of the disease; other influencing factors between infection and HDL levels need to be further explored.…”
Section: Association Between M Pneumoniae Infection and Hdl Metabolismmentioning
confidence: 99%
“…In addition, these infections show seasonal epidemics, usually peaking in winter and early spring (7). M. pneumoniae infection can change the blood lipid content of patients and accelerate occurrence and development of cardiovascular diseases such as coronary heart disease and atherosclerosis (8)(9)(10).…”
The association between
Mycoplasma pneumoniae
(
M. pneumoniae
) infection, high-density lipoprotein metabolism and cardiovascular disease is an emerging research area. The present review summarizes the basic characteristics of
M. pneumoniae
infection and its association with high-density lipoprotein and cardiovascular health.
M. pneumoniae
primarily invades the respiratory tract and damages the cardiovascular system through various mechanisms including adhesion, invasion, secretion of metabolites, production of autoantibodies and stimulation of cytokine production. Additionally, the present review highlights the potential role of high-density lipoprotein for the development of prevention and intervention of
M. pneumoniae
infection and cardiovascular disease, and provides suggestions for future research directions and clinical practice. It is urgent to explore the specific mechanisms underlying the association between
M. pneumoniae
infection, high-density lipoprotein metabolism, and cardiovascular disease and analyze the roles of the immune system and inflammatory response.
“…Worldwide, cardiovascular disease (CVD) is the number one cause of death and premature death (Kivimäki and Steptoe, 2018;Kovacic et al, 2019;Silva et al, 2015;Singh et al, 2020;Yang et al, 2021). A chronic inflammatory lipid-depositing disease causes peripheral artery disease, coronary artery disease, and myocardial infarction (Gao and Liu 2017).…”
Kirenol (KNL) has recently been reported to have anti-inflammatory properties. Yet, little is known about the potential mechanisms of its anti-inflammatory properties. In HUVECs, we elucidated the anti-inflammatory mechanisms of kirenol. RT-PCR was used to test mRNA of pro-inflammatory mediators produced by Ox-LDL. The viability of cells was measured using MTT. Western blots analyzed protein levels. On Ox-LDL-stimulated HUVECs, KNL significantly inhibited the production of pro-inflammatory mediators such as NO, IL-1β, iNOS, TNF-α and IL-6. p38, ROS and Nrf2 expression were inhibited by KNL. Inhibition of p38, ROS, and KNL caused nuclear accumulation of Nrf2. KNL attenuated Ox-LDL-induced phosphorylation of ERK1/2 and p38, too. Based on our results, KNL inhibits NF-кB and MAPK signaling in HUVECs by activating Nrf2 signaling. There's a possibility that KNL could be developed into an anti-inflammatory drug.
“…The resulting deaths of coronary artery disease (CAD) by year 2030 will reach about 23.6 million people which majority will be from South Asia (Saha et al, 2021). Due to this high prevalence and high mortality, this disease has received a lot of attention in recent decades and so far, many studies have been conducted on pathophysiology (Shah et al, 2022), prevalence and risk factors for coronary heart disease (CHD) (Dugani et al, 2021;Yang et al, 2021).…”
Background
The COVID-19 pandemic has increased psychological distress and impacted diagnosis and treatment of noncommunicable diseases. This study aimed to examine the comparative effectiveness of Emotionally Focused Therapy (EFT) and Transcranial Direct Current Stimulation (tDCS) on anxiety and quality of life in patients with coronary artery disease (CAD) during COVID-19 pandemic.
Methods
A total of forty-five participants who met criteria for a current episode of CAD chosen by convenience sampling method from Tehran city were randomly assigned to a 9-week/60-min EFT (n = 15) group therapy, 5-week/20-min tDCS (n = 15) experimental group and one control group (n = 15). They were assessed at pre-treatment, post-group, and 3-month follow-up. The study subjects completed the self-reported questionnaires, Beck Anxiety Inventory (BAI) and Health-Related Quality of Life (HRQOL).
Results
Repeated measures analysis of variance, ANOVA, was used to measure inferential statistics. There were significant improvements in Anxiety and Quality of Life scores in both EFT and tDCS groups over the post and follow-up period (P > 0.05). However, difference was found when EFT had a greater effect on Anxiety and Quality of Life.
Conclusions
These results showed EFT and tDCS have effective interventions in reducing anxiety and improving the quality of life of CAD patients, but improvements with EFT were greater than those with tDCS.
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