Related Experiment Video
Updated: May 11, 2026

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
Published on: March 22, 2017
Identification and validation of differentially expressed disulfidptosis-related genes in hypertrophic cardiomyopathy
Huimin Fan1, Xin Tan2,3, Shuai Xu2,3
1Center of Translational Medicine and Clinical Laboratory, Suzhou Dushu Lake Hospital, The Fourth Affiliated Hospital to Soochow University, Suzhou, 215000, China.
Insights
This study explores disulfidptosis, a novel cell death mechanism, in hypertrophic cardiomyopathy (HCM). Researchers developed a predictive model using disulfidptosis-related genes for potential HCM biomarkers and therapeutic targets.
Area of Science:
- Cardiovascular Research
- Cell Death Mechanisms
- Biomarker Discovery
Background:
- Hypertrophic cardiomyopathy (HCM) is a prevalent cardiovascular disease with complex origins and limited treatment options.
- Disulfidptosis, a recently identified form of programmed cell death, has been primarily investigated in cancer, with its role in cardiovascular diseases largely unexplored.
Purpose of the Study:
- To investigate the potential association between disulfidptosis and the pathogenesis of hypertrophic cardiomyopathy.
- To develop a predictive model for HCM utilizing genes associated with disulfidptosis.
- To identify potential therapeutic strategies targeting disulfidptosis pathways in HCM.
Main Methods:
- Development of a predictive model using Support Vector Machine (SVM) machine learning.
- Identification of key disulfidptosis-related genes (DRGs) including GYS1, MYH10, PDMIL1, SLC3A2, and CAPZB.
- Validation of findings in a Transverse Aortic Constriction (TAC) mouse model using western blot, RNA sequencing, and immunohistochemistry.
- Utilized the Comparative Toxicogenomics Database (CTD) to identify potential therapeutic agents.
Main Results:
- A predictive model incorporating specific DRGs demonstrated high performance in identifying HCM.
- The study validated the presence and relevance of disulfidptosis-associated genes in a mouse model of cardiac hypertrophy.
- Resveratrol was identified as a potential therapeutic agent targeting core genes involved in disulfidptosis within the context of HCM.
Conclusions:
- Disulfidptosis represents a novel area of investigation for understanding hypertrophic cardiomyopathy.
- The identified DRGs and the predictive model offer promising avenues for biomarker discovery in HCM.
- Resveratrol emerges as a potential therapeutic candidate for targeting disulfidptosis in hypertrophic cardiomyopathy, warranting further clinical investigation.
Abstract:
Hypertrophic cardiomyopathy (HCM) is one of the most common cardiovascular diseases with no effective treatment due to its complex pathogenesis. A novel cell death, disulfidptosis, has been extensively studied in the cancer field but rarely in cardiovascular diseases. This study revealed the potential relationship between disulfidptosis and hypertrophic cardiomyopathy and put forward a predictive model containing disulfidptosis-associated genes (DRGs) of GYS1, MYH10, PDMIL1, SLC3A2, CAPZB, showing excellent performance by SVM machine learning model. The results were further validated by western blot, RNA sequencing and immunohistochemistry in a TAC mice model. In addition, resveratrol was selected as a therapeutic drug targeting core genes using the CTD database. In summary, this study provides new perspectives for exploring disulfidptosis-related biomarkers and potential therapeutic targets for hypertrophic cardiomyopathy.

