Search

CN-122005803-A - Application of OLA1 as target in preparing medicines for inhibiting myocardial fibrosis

CN122005803ACN 122005803 ACN122005803 ACN 122005803ACN-122005803-A

Abstract

The application provides application of OLA1 as a target in preparing medicines for inhibiting myocardial fibrosis, relates to the technical field of biomedicine, and aims at solving the problems that pathogenesis of myocardial fibrosis is not completely clear and treatment means is deficient in the prior art. Based on the above, the application provides that the OLA1 inhibitor (including small molecule compounds, siRNA and the like) is used for preparing medicines for treating myocardial fibrosis, and provides a new therapeutic strategy for clinic. According to the application, the direct association of the OLA1 gene and the pathological process of myocardial fibrosis is disclosed for the first time, and the gene knockout experiment proves that inhibiting OLA1 can obviously improve myocardial fibrosis and provides a new direction for developing targeted drugs.

Inventors

  • MAO RENFANG
  • HU ZIXUAN
  • YANG HAO
  • FAN YIHUI

Assignees

  • 南通大学

Dates

Publication Date
20260512
Application Date
20260211

Claims (8)

  1. The application of OLA1 serving as a target in preparing medicaments for inhibiting myocardial fibrosis is characterized in that the sequence of the OLA1 is shown as SEQ ID NO. 01.
  2. 2. The use of OLA1 as target in the manufacture of a medicament for inhibiting myocardial fibrosis according to claim 1, wherein the medicament is for inhibiting expression of OLA1 gene.
  3. 3. The use of OLA1 as target in the preparation of a medicament for inhibiting myocardial fibrosis, wherein the medicament comprises at least one of siRNA, CRISPR and small molecule compound for inhibiting OLA1 gene expression.
  4. 4. The use of OLA1 as target in the preparation of a medicament for inhibiting myocardial fibrosis according to claim 3, wherein the small molecule compound is selected from RNA interfering agents, antisense oligonucleotides or OLA1 protein inhibitors.
  5. 5. The use of OLA1 as target in the manufacture of a medicament for inhibiting myocardial fibrosis according to claim 4, wherein the medicament further comprises pharmaceutically acceptable adjuvants.
  6. 6. A drug for inhibiting myocardial fibrosis, characterized in that the drug inhibits myocardial fibrosis by inhibiting the expression of OLA 1.
  7. 7. A pharmaceutical composition for inhibiting myocardial fibrosis according to claim 6, wherein the composition contains at least one of siRNA, CRISPR and small molecule compound for inhibiting OLA1 gene expression.
  8. 8. A pharmaceutical composition for inhibiting myocardial fibrosis according to claim 7, wherein the composition further includes pharmaceutically acceptable adjuvants.

Description

Application of OLA1 as target in preparing medicines for inhibiting myocardial fibrosis Technical Field The application relates to the technical field of biomedicine, in particular to application of OLA1 serving as a target in preparation of medicines for inhibiting myocardial fibrosis. Background Myocardial fibrosis is a common cardiac pathophysiological process characterized by excessive deposition of extracellular matrix (ECM) components of the heart and abnormal remodeling. Under normal circumstances, the extracellular matrix is mainly composed of collagen, elastin, proteoglycans, glycosaminoglycans, and the like, which together maintain the structure and function of the heart. However, in the progress of various heart diseases (such as hypertensive heart disease, ischemic heart disease, myocarditis, cardiac hypertrophy, etc.), cardiac fibrosis gradually occurs and aggravates, leading to increased stiffness of the heart, reduced compliance, and finally possibly causing serious consequences such as heart failure, etc., which seriously affect the quality of life and survival rate of patients. The mechanism by which myocardial fibrosis occurs is complex, involving the interaction of multiple cell types and signaling pathways. Among them, injury and death of cardiomyocytes are one of the key factors that initiate myocardial fibrosis. When the cardiomyocytes are stimulated by factors such as ischemia, hypoxia, inflammation, etc., a range of cytokines and chemokines such as transforming growth factor-beta (TGF-beta), angiotensin II (AngII), interleukin-1 (IL-1), etc., are released. These factors are capable of activating cardiac fibroblasts, transforming them from a resting state to an activated state with synthesis and secretion functions, synthesizing and secreting a large amount of extracellular matrix components, in particular collagen. In addition, oxidative stress, endoplasmic reticulum stress, mechanical stress, etc. also play an important role in the progression of myocardial fibrosis, which promotes excessive accumulation and remodeling of extracellular matrix through various pathways. At present, the treatment means for myocardial fibrosis are relatively limited in clinic, and the effect is not ideal. Traditional therapeutic strategies include mainly treatments for primary diseases, such as controlling blood pressure, improving myocardial blood supply, anti-inflammatory, etc. For example, for patients with hypertension, the use of antihypertensive drugs (such as ACE inhibitors, angiotensin receptor antagonists, etc.) can slow down the progression of myocardial fibrosis to some extent, and for patients with ischemic heart disease, coronary intervention or coronary bypass surgery can improve myocardial blood supply, alleviate myocardial ischemia injury, and thus produce a certain inhibition of myocardial fibrosis. In addition, some drugs such as aldosterone antagonists, beta blockers, and the like are also used in the treatment of myocardial fibrosis, but the mechanism of action of these drugs is primarily by improving the hemodynamic state of the heart or alleviating the over-activation of the neuroendocrine system. The current treatment methods have weak direct inhibition effect on myocardial fibrosis, and have a plurality of limitations, so that a new treatment target is needed to be discovered for treating myocardial fibrosis. Disclosure of Invention The application aims to provide a novel therapeutic target, and myocardial fibrosis is effectively inhibited through the discovery of the novel therapeutic target. In order to achieve the above object, the present application provides the following technical solutions: the application of OLA1 as a target in preparing medicaments for inhibiting myocardial fibrosis is provided, wherein the sequence of the OLA1 is shown as SEQ ID NO. 01. Preferably, the medicament is for inhibiting expression of OLA1 gene. Preferably, the medicament comprises at least one of siRNA, CRISPR and small molecule compound for inhibiting the expression of OLA1 genes. Preferably, the small molecule compound is selected from the group consisting of an RNA interference agent, an antisense oligonucleotide, or an OLA1 protein inhibitor. Preferably, the medicament further comprises other auxiliary agents which are acceptable in medicine. The present application also provides a medicament for inhibiting myocardial fibrosis by inhibiting expression of OLA 1. Preferably, the medicament comprises at least one of siRNA, CRISPR and small molecule compound for inhibiting the expression of OLA1 genes. Preferably, the medicament further comprises other auxiliary agents which are acceptable in medicine. Compared with the prior art, the application at least comprises the following beneficial effects: The application reveals the direct association of the OLA1 gene and the pathological process of myocardial fibrosis for the first time, and the myocardial fibrosis prognosis can be obviously improv