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Global Translational Medicine Effect of leptin on aortic dissection

serious cardiovascular and cerebrovascular diseases . In inevitably lead to a series of changes in cell function,
[6]
a study, abundant inflammatory cytokines were detected which will have an irreversible impact on cell metabolism,
in adipocytes, and adipose tissue was found to have an cell self-renewal, and cell life cycle [27-33] . For example, in
effect on the oxidative stress reaction in AD patients by AD, the expression of autophagy in the middle layer was
releasing large amounts of polypeptides and cytokines into found to be significantly higher than that in the control
the blood circulation, thus inducing the occurrence and group, thus suggesting the overactivation of autophagy
[27]
development of various diseases . A number of studies in AD . Studies have confirmed that MYH11, a myosin
[15]
have also pointed out that lipid metabolism is involved marker of SMCs, leads to autophagic conversion through
in aortic vascular remodeling and further confirmed that the ubiquitin-proteasome system after being stimulated
obesity has a strong correlation with the occurrence and by the external environment [28,29] . In a study, adult mice
development of abdominal aortic aneurysm and AD [18-20] . that lack autophagy died of hypoglycemia 24 h after
Relevant research has confirmed this hypothesis laterally. starvation, indicating that autophagy plays a key role in
[30]
Studies have found that insulin resistance (5.5% ≤ HbA1c glucose homeostasis . In addition, studies have shown
≤ 6.5%), caused by abnormal glucose metabolism, had that the phenotypic transformation of SMCs, induced by
[27]
significantly increased the cardiovascular incidence rate PDGF, can be inhibited by inhibiting autophagy levels .
in this population [21,22] . The studies have also pointed out Moreover, glucose is known to regulate the autophagy level
[31]
that insulin resistance is the main feature of pre-diabetes, in organisms by controlling glucagon/insulin secretion .
which can cause hyperlipidemia syndrome with elevated The inflammatory reaction and vascular fibrosis that are
plasma triglyceride (TG), reduced human low-density induced by abnormal glucose and lipid metabolism can
lipoprotein (HLDL), and elevated very low-density promote the occurrence and development of AD. It has
lipoprotein (VLDL). Obesity is one of the main risk been found that macrophages can infiltrate the aortic wall
factors for insulin resistance . The inflammatory reaction and release matrix metalloproteinases that degrade the
[19]
caused by excessive fat accumulation and abnormal lipid elastic fibers of the aortic wall, which, in turn, decreases the
metabolism may eventually lead to insulin resistance. It is elasticity of the vascular wall. Eventually, the middle layer
evident that there is a close relationship between lipid and of the aortic wall degenerates and loses its elasticity, causing
[32]
glucose metabolism. vascular tears under the stimulation of hypertension .
In view of the excessive fibrotic and brittle nature of the
Relevant studies have shown that glucose and lipid aortic wall as a result of the stimulation of inflammatory
metabolism play an important role in the phenotypic factors, the aortic wall is unable to withstand the shear
transformation of SMCs [22-24] . The phenotype of aortic force generated by blood pressure, which eventually causes
SMCs in AD patients changes from contractile to dissection .
[33]
secretory, which is accompanied by increased glycolytic
flux, decreased glucose oxidation, and increased Leptin is closely related to glucose and lipid metabolism.
cholesterol [19,24,25] . Moreover, the increase in insulin Leptin plays an important role in the regulation of glucose
resistance and lactate dehydrogenase A (LDHA) levels and lipid metabolism, energy metabolism, reproductive
can induce the phenotypic transformation of SMCs and development, and immune regulation by acting on the
promote the occurrence of AD. However, the study also central nervous system and peripheral tissues. Leptin is an
found that the occurrence and development of AD are independent predictor of carotid intima-media thickness
[34]
greatly inhibited by drug intervention or the inhibition of (cIMT) in obese patients . Similar associations have been
[35]
these processes [20,26] . found in healthy male and female individuals , obese
children , and psoriasis patients [37,38] . In addition, the
[36]
In addition, abnormal glucose and lipid metabolism presence of carotid plaque is associated with hyperleptinemia
also affect a variety of physiological processes, including in patients with systemic lupus erythematosus (SLE) .
[39]
autophagy, inflammatory reaction, and vascular fibrosis, With regard to the severity of carotid artery disease, high
all of which play an important role in the progression of leptin concentration has been found to be associated with
AD. The abnormal metabolism of glucose and lipid plays plaque instability characteristics in carotid endarterectomy
different roles in different stages of arterial dissection. patients . Furthermore, the overexpression of leptin
[40]
Hyperglycemia in patients (diabetes), to a certain extent, receptor gene (LEPR) has been observed in advanced
provides the energy source for blood vessels. In some ways, carotid atherosclerosis . The previous studies, however,
[41]
this is beneficial to the stability of the disease, but long- have reported that leptin concentration in symptomatic
term hyperglycemia promotes vascular inflammation and carotid artery disease patients was lower than that in
fibrosis and ultimately leads to vascular abnormalities. asymptomatic patients . In a rat carotid artery injury
[42]
The abnormality of glucose and lipid metabolism will model, genistein (an isoflavone) has been found to

Volume 1 Issue 2 (2022) 6 https://doi.org/10.36922/gtm.v1i2.85