SRSF1 Targeting in Vascular Smooth Muscle for Aortic Dissection
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Solution Overview
Problem
Current treatments for aortic dissection are limited, with no effective drugs available to prevent or treat this life-threatening condition, and surgical interventions are costly and risky.
Innovation Solution
Utilizing SRSF1 as a therapeutic target, specifically through SRSF1 inhibitors such as nucleic acid molecules and protein inhibitors, to regulate SRSF1 expression and inhibit aortic dissection.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If surgical intervention is used to treat aortic dissection, then the condition can be addressed, but the treatment is difficult, expensive, and associated with high mortality and disability rates
Solution Approach 1:
The patent replaces mechanical surgical intervention with a biochemical therapeutic approach by identifying SRSF1 as a molecular target. Small molecules or biologics can be designed to inhibit SRSF1 function, thereby preventing aortic dissection through molecular mechanisms rather than physical surgery. This substitution reduces the harmful effects associated with surgical procedures while maintaining treatment effectiveness.
Solution Approach 2:
The patent introduces SRSF1 as an intermediary molecular target that mediates the pathological process of aortic dissection. By targeting this specific protein involved in extracellular matrix metabolism and vascular smooth muscle cell function, the treatment can intervene in the disease process at a molecular level, providing a less invasive alternative to surgery with reduced mortality and disability risks.
2Adaptability or versatility
If no pharmacological treatment is available for aortic dissection, then surgical options remain, but drug-free treatment limits are severe and preventive therapy is unavailable
Solution Approach 1:
The patent enables preliminary preventive action by identifying SRSF1 as a target that can be inhibited before aortic dissection occurs. Pharmacological agents targeting SRSF1 can be administered to high-risk patients to prevent the development of aortic dissection, rather than only treating it after surgical intervention becomes necessary. This preliminary pharmacological intervention expands treatment versatility and provides reliable preventive capability.
3Ease of manufacture
If the pathogenesis of aortic dissection remains unclear, then targeted therapy cannot be developed, but this lack of understanding prevents effective treatment development
Solution Approach 1:
The patent extracts and isolates SRSF1 as a specific molecular target from the complex pathogenesis of aortic dissection. By focusing on this single protein's role in extracellular matrix metabolism and vascular smooth muscle cell function, the research transforms the unclear overall pathogenesis into a well-defined molecular target, enabling feasible drug development while recovering the lost information about disease mechanisms.
Data Source
AI summary
Use of a serine/arginine-rich splicing factor 1 (SRSF1) as a therapeutic target for aortic dissection is provided, which belonging to the technical field of biomedicine. The SRSF1 can be used as a target to screen a drug for preventing and/or treating aortic dissection. SRSF1 expression is upregulated in both β-aminopropionitrile (BAPN)-induced aortic dissection model mice and aortic dissection patients. Mice with SRSF1 knockdown in vascular smooth muscle cells (VSMCs) are less susceptible to aortic dissection and elastic fiber degradation induced by BAPN. Mice with high expression of SRSF1 in VSMCs are more susceptible to aortic dissection and elastic fiber degradation induced by BAPN. Mechanistically, the SRSF1 can regulate the inflammatory phenotype of vascular smooth muscle and promote the degradation of vascular extracellular matrix. Knocking down the SRSF1 may improve the above phenomenon, thereby providing a new target for the treatment of aortic dissection.