Regnase-1 Biomarker and PAH Model for Pulmonary Hypertension Testing
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Solution Overview
Problem
Current methods for diagnosing and treating pulmonary hypertension, particularly pulmonary arterial hypertension (PAH), lack effective markers and models for assessing disease presence, severity, and prognosis, and require harsh conditions for drug screening.
Innovation Solution
Utilizing Regnase-1 as a marker for pulmonary hypertension and creating a PAH model animal with immune cell-specific Regnase-1 deficiency, which spontaneously develops PAH, allowing for drug screening and assessment without hypoxia or chemical exposure, and employing oligonucleic acids to disrupt Regnase-1 mRNA stem-loop structures for therapeutic intervention.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If traditional methods (hypoxia load, chemical substance exposure) are used to create PAH model animals, then PAH can be induced, but the methods are harsh and complex
Solution Approach 1:
The patent extracts the essential pathogenic mechanism of PAH by identifying Regnase-1 deficiency in immune cells as the critical factor, eliminating the need for harsh external inducers like hypoxia or chemicals. This allows spontaneous PAH development in a controlled genetic model.
Solution Approach 2:
The model animal system serves itself by spontaneously developing PAH through its inherent Regnase-1 deficiency without requiring external intervention. The disease progresses naturally within the model, providing a self-sustaining system for drug screening.
2Ease of operation
If Regnase-1 deficiency is introduced in immune cells, then PAH develops spontaneously, but the mechanism becomes more complex
Solution Approach 1:
The patent segments the complex PAH pathogenesis by focusing specifically on immune cell Regnase-1 deficiency as the primary driver, separating this mechanism from other potential contributing factors. This segmentation simplifies the model while maintaining relevance to human PAH.
3Reliability
If Regnase-1 expression is suppressed therapeutically, then PAH symptoms improve, but the mechanism of action becomes less understood
Solution Approach 1:
The patent establishes a feedback loop where Regnase-1 deficiency is identified as the therapeutic target, and suppression of Regnase-1 expression provides measurable improvement in PAH symptoms. This feedback validates the therapeutic mechanism while guiding future research directions.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
Enables accurate diagnosis and prognosis of pulmonary hypertension, provides a reliable PAH model for drug screening, and offers therapeutic options by suppressing Regnase-1 expression to improve clinical outcomes.
Implementation Method 1
a substance that disrupts a stem-loop structure in the 3′UTR of Regnase-1 mRNA... an oligonucleic acid that hybridizes to at least a part of a base sequence in a region that forms a stem-loop structure
Data Source
AI summary
A purpose of the present disclosure is to provide a method for testing presence/absence, severity or prognosis of pulmonary hypertension; a pathological model animal for pulmonary arterial hypertension; and a prophylactic or therapeutic drug for hypertension. Provided are: a testing method for hypertension, with Regnase-1 used as a biomarker; a PAH pathological model animal consisting of a non-human animal with Regnase-1 deficiency in alveolar macrophage; and a prophylactic or therapeutic drug for hypertension, containing a substance that disrupts a stem-loop structure in 3′UTR of Regnase-1 mRNA.