MicroRNA Modulation for Post-Myocardial Infarction Remodeling

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Solution Overview

Problem

Current treatments for myocardial infarction and heart failure do not effectively address the post-myocardial infarction remodeling process, which leads to further cardiac damage and potential life-threatening arrhythmias, with no known therapeutic interventions available to manage this aspect of heart disease.

Innovation Solution

Modulation of specific microRNAs (miRNAs) such as let-7 family members, miR-15b, miR-21, miR-199a, and others, through the use of inhibitors or agonists, to regulate their expression or activity in heart cells, thereby treating or preventing myocardial infarction, cardiac remodeling, and heart failure.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If current treatments for myocardial infarction are used, then immediate cardiac damage is addressed, but post-myocardial infarction remodeling is not effectively managed leading to further cardiac damage

Engineering Contradiction:
Improveeffectiveness of treatmentVSAvoidcoverage of disease stages
Core Design Contradiction:
ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent segments the treatment approach by identifying and targeting specific microRNAs (such as miR-21, miR-29, miR-1) that are differentially expressed during post-MI remodeling. This allows for stage-specific and mechanism-specific therapeutic intervention, addressing the remodeling process separately from acute infarct management.

Inventive Principle:
Principle #1Segmentation

Solution Approach 2:

The patent employs parameter changes by modulating microRNA expression levels (upregulating protective miRNAs like miR-29 and downregulating harmful miRNAs like miR-21) to control the remodeling process. This molecular-level parameter adjustment provides a new dimension for therapeutic intervention.

Inventive Principle:
Principle #35Parameter changes

2Device complexity

If no therapeutic intervention is applied to post-MI remodeling, then treatment complexity is low, but fibrosis and arrhythmias increase

Engineering Contradiction:
Improvetreatment complexityVSAvoidfibrosis and arrhythmias
Core Design Contradiction:
Device complexityVSObject-affected harmful factors

Solution Approach 1:

The patent uses microRNAs as intermediary molecules to mediate the therapeutic effect. These small non-coding RNAs serve as intermediaries between the administered therapy and the target genes involved in remodeling, fibrosis, and arrhythmia development, providing a controlled mechanism for disease modification.

Inventive Principle:
Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent applies preliminary action by intervening in the remodeling process before irreversible damage occurs. By targeting microRNA expression early in the remodeling phase, the therapy prevents the development of severe fibrosis and arrhythmias before they become life-threatening conditions.

Inventive Principle:
Principle #10Preliminary action

3Reliability

If microRNA modulation is implemented, then therapeutic effectiveness improves, but treatment mechanism complexity increases

Engineering Contradiction:
Improvetherapeutic effectivenessVSAvoidtreatment mechanism
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent extracts and isolates specific microRNA molecules (such as miR-21, miR-29, miR-1) from the complex cellular environment and uses them as discrete therapeutic agents. This extraction approach simplifies the treatment mechanism by focusing on key regulatory molecules rather than attempting to modulate the entire gene expression network.

Inventive Principle:
Principle #2Taking out (Extraction)

Data Source

PatentUS9072765B2Identification of micro-RNAs involved in post-myocardial infarction remodeling and heart failure
Publication Date: 2015.07.07 BOARD OF RGT THE UNIV OF TEXAS SYST
  • US9072765B2 patent drawing
  • US9072765B2 patent drawing
  • US9072765B2 patent drawing

AI summary

The present invention relates to the identification of miRNAs that are involved in heart failure and the process of post-myocardial infarction remodeling in heart tissue. Modulation of these identified miRNAs as a treatment for myocardial infarction, cardiac remodelling, and heart failure is described.