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Global Translational Medicine Effect of leptin on aortic dissection

Stanford classification divides AD into two types. are the main types of metabolic syndrome (MetS). MetS
In type A, the rupture of intima may be located in the is characterized by abdominal obesity and abnormal
ascending aorta, aortic arch, or proximal descending aorta. metabolism of lipids, glucose, and carbohydrate, which
The scope of dissection involves the ascending aorta, the may cause a series of cardiovascular and cerebrovascular
aortic arch, descending aorta, and even the abdominal diseases .
[12]
aorta. In type B, the rupture of intima is often located in In recent years, research on the mechanism of
the proximal descending aorta. The scope of dissecting AD has mainly focused on hypertension and changes
aneurysm is limited to the descending aorta or extends into in metalloproteinases, among which leptin plays an
the abdominal aorta; it does not affect the ascending aorta. important role. Leptin is a hormone that is mainly secreted
The most important clinical features of Stanford type A by adipocytes and involved in the control of food intake
dissection are its acute onset and rapid progress. In clinical through its action on the hypothalamus, leading to the
practice, we have found that the early diagnosis rate of AD suppression of appetite . Further research on leptin
[13]
is low, and some patients die of an aortic rupture before a
definite diagnosis is made. Emergency surgery is the only has found that the hormone not only has a variety of
effective treatment for acute Stanford type A dissection. endocrine functions but also participates in immune and
Although the surgical technology for acute Stanford inflammatory responses, hematopoiesis, angiogenesis,
type A dissection has made significant advancements reproduction, gene expression of cell cycle regulation,
[8,9,14]
in recent years with the continuous progress of science and regulation of cell matrix remodeling . Leptin also
and technology, such as the three-branch vascular stent participates in the decomposition of the extracellular
technology used in aortic arch reconstruction and other matrix (ECM), promotes angiogenesis, and improves the
technologies that improve the safety of AD surgery and mitotic activity of vascular endothelial cells by regulating
[5]
the prognosis of patients, the difficulty of surgery still poses the expression of matrix metalloprotein (MMP)-9 and
[15]
a challenge, and the risk of mortality is still high. Usually, tissue inhibitors of metalloproteinases (TIMPs) . This
only large, well-equipped heart centers are able to carry suggests that leptin may be involved in the occurrence of
out such emergency operations. The majority of patients AD. However, only a number of clinical trials have studied
need to be transferred to large heart centers for surgical the role of leptin in AD thus far. Therefore, the role that
treatment after a concrete diagnosis is made, among which leptin plays in AD patients remains unclear.
some patients may die during the transfer. Therefore, it is Several research groups all over the world have adopted
of great significance to explore the molecular mechanism animal models to study the impact of leptin on the
of AD and find potential therapeutic targets for the occurrence and development of AD. The results of these
prevention and treatment of this life-threatening disease. pre-clinical studies are often derived from a relatively
The exact pathogenesis of AD is unclear. At present, small sample, and there is no objective or quantitative
it is generally believed that AD is formed on the basis of way to systematically evaluate and summarize all the
the internal causes of the arterial wall itself in addition studies. Therefore, we present a systematic review and
to a series of external factors, such as hypertension, meta-analysis of leptin in AD animal models to clarify the
trauma, and so on. AD often occurs in patients with relationship between leptin and AD.
idiopathic degeneration of the middle layers of the aorta
and certain hereditary diseases, such as Marfan syndrome, 2. Materials and method
Ehlers-Danlos syndrome, Turner syndrome, and other 2.1. Materials
connective tissue disorders. This is due to the internal We conducted a computerized literature search on animal
factor of weak aortic wall in these patients. In the process studies related to leptin and AD in PubMed, EMBASE,
of AD formation, the external factors that cause tearing Cochrane Library, MEDLINE, and other databases from
of the intima and promote high-speed blood flow into their inception to present. The keywords used were “Leptin,”
the middle layer play important roles. These external “Obese Protein,” “Obese Gene Product, “Gene Product,
factors include arterial blood pressure, wall shear stress, Obese,” “Ob Gene Product,” “Gene Product, Ob,” “Ob
and hemodynamic status [6,7] . However, AD is not caused
merely by the stimulation of these external factors; Protein,” “Aneurysm,” “Aneurysms,” “Fusiform Aneurysm,”
instead, the primary cause of AD is the weakness of the “Aneurysm, Fusiform,” “Aneurysms, Fusiform,” “Fusiform
aortic wall itself. The weakness of the aortic wall has been Aneurysms,” and “Saccular Aneurysm.”
relentlessly investigated. Some studies have pointed out The titles and abstracts of the identified studies were
that the weakness of the aortic wall may be closely related scanned to exclude any study that was irrelevant. The full
to abnormal glucose and lipid metabolism [8-11] , which texts of the remaining articles were read to determine

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