2018
DOI: 10.1016/j.ajem.2017.12.032
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A novel biochemical marker for predicting the severity of ACS with unstable angina pectoris: Asprosin

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Cited by 49 publications
(41 citation statements)
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“…Asprosin in the circulation could cross the blood-brain barrier and directly activate orexigenic Agouti-related peptide neurons through a cyclic adenosine monophosphate-dependent pathway, leading to appetite stimulation and a drive to accumulate adiposity and bodyweight 17,18 . Acara et al 19 suggested that asprosin might be a novel biochemical marker for predicting the severity of acute coronary syndrome with unstable angina pectoris. Wang et al 20 showed that higher asprosin concentrations before bariatric surgery were associated with the weight reduction magnitude at 6 months after surgery.…”
Section: Discussionmentioning
confidence: 99%
“…Asprosin in the circulation could cross the blood-brain barrier and directly activate orexigenic Agouti-related peptide neurons through a cyclic adenosine monophosphate-dependent pathway, leading to appetite stimulation and a drive to accumulate adiposity and bodyweight 17,18 . Acara et al 19 suggested that asprosin might be a novel biochemical marker for predicting the severity of acute coronary syndrome with unstable angina pectoris. Wang et al 20 showed that higher asprosin concentrations before bariatric surgery were associated with the weight reduction magnitude at 6 months after surgery.…”
Section: Discussionmentioning
confidence: 99%
“…By comparing the levels of asprosin and the scoring system, a study showed that the changes in the levels of asprosin were positively correlated with the Syntax score. This suggested that asprosin could be a viable marker for unstable angina pectoris (UAP), and the severity of acute coronary syndrome (ACS) with UAP might be predicted by it (33).…”
Section: Asprosin In Cvdmentioning
confidence: 99%
“…On the other hand, in pre-STZ group a significant (p<0.001) decrease in serum levels of glucose, TC, TG, LDL, VLDL, TNF α , % HbA1c and Introduction ASPROSIN, a protein hormone, was discovered by Romere, Duerrschmid [1] and shared in regulation of glucose homeostasis. It is the C-terminal cleavage product of profibrillin and is regulated with the starvation and causes hepatic glucose release by activating hepatic G protein-cAMP-PKA way [2] . Kader, Meltem [3] found that asprosin deficiency in human caused lipodystrophy with reduced plasma insulin.…”
mentioning
confidence: 99%
“…Wang, Qu [4] stated that adipose tissue is considered as an endocrine organ secreting adipokines as asprosin, which participated in the pathologic processes of diabetes mellitus. Asprosin was named after the Greek word for white (aspros), because of the decrease in subcutaneous white adipose tissue that was found in asprosin-deficient patients and because white adipose tissue is a source of plasma asprosin [2] . It was found that plasma asprosin displayed circadian oscillation with an acute drop in levels coinciding with the onset of feeding, while, overnight fasting and insulin resistance increased its circulating levels [1,2] .…”
mentioning
confidence: 99%
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