Current drug targets · 2026
Transcriptomic Profiling Identifies MyD88 and Pik3r3 as Hub Genes Associated with the Anti-hypertrophic Effects of B-type Natriuretic Peptide.
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Wu Changchun, Wang Yaqing, Zhang Zixuan, He Chen, Feng Haiyan, Sun Zhipeng, Ren Dongsheng, Du Mengze, Huang Jian
Аннотация
INTRODUCTION: B-type natriuretic peptide (BNP) is widely used to diagnose and assess heart failure prognosis. However, its effects on pathological cardiomyocyte hypertrophy and the underlying mechanisms remain largely unexplored.
METHODS: Here, we report the use of isoproterenol (ISO)-induced cardiomyocyte hypertrophy models with varying doses of BNP to investigate the potential targets and molecular mechanisms of BNP in rat cardiomyocyte hypertrophy.
RESULTS: Phenotypic measurement confirmed that BNP treatment significantly attenuated ISOinduced cardiomyocyte hypertrophy. Transcriptomic profiling of cardiomyocytes identified key markers and pathways associated with hypertrophy and BNP intervention, revealing that BNP could broadly reverse ISO-induced molecular perturbations. Trajectory analysis and network module analysis further highlighted MyD88 and Pik3r3 as candidate regulatory nodes associated with BNP intervention. BNP treatment potentially downregulates these genes, which is accompanied by reduced activity of inflammatory and growth-related signaling networks. These changes are associated with pathways involved in sarcomeric protein synthesis, immune-inflammatory responses, myocardial fibrosis, mitochondrial homeostasis, and oxidative stress, suggesting a potential role for BNP in attenuating cardiomyocyte hypertrophy.
DISCUSSION: These findings suggest that BNP may exert protective effects against cardiomyocyte hypertrophy through coordinated modulation of multiple signaling pathways. MyD88- and Pik3r3- associated networks emerged as potential molecular mechanisms underlying BNP-mediated responses and may represent promising targets for future investigation.
CONCLUSION: This study provides transcriptomic evidence that BNP may attenuate cardiomyocyte hypertrophy and identifies MyD88- and Pik3r3-associated signaling networks as potential molecular mediators of this response. These findings suggest possible mechanisms underlying the protective effects of BNP and provide a foundation for future functional validation studies in hypertrophic heart disease.
METHODS: Here, we report the use of isoproterenol (ISO)-induced cardiomyocyte hypertrophy models with varying doses of BNP to investigate the potential targets and molecular mechanisms of BNP in rat cardiomyocyte hypertrophy.
RESULTS: Phenotypic measurement confirmed that BNP treatment significantly attenuated ISOinduced cardiomyocyte hypertrophy. Transcriptomic profiling of cardiomyocytes identified key markers and pathways associated with hypertrophy and BNP intervention, revealing that BNP could broadly reverse ISO-induced molecular perturbations. Trajectory analysis and network module analysis further highlighted MyD88 and Pik3r3 as candidate regulatory nodes associated with BNP intervention. BNP treatment potentially downregulates these genes, which is accompanied by reduced activity of inflammatory and growth-related signaling networks. These changes are associated with pathways involved in sarcomeric protein synthesis, immune-inflammatory responses, myocardial fibrosis, mitochondrial homeostasis, and oxidative stress, suggesting a potential role for BNP in attenuating cardiomyocyte hypertrophy.
DISCUSSION: These findings suggest that BNP may exert protective effects against cardiomyocyte hypertrophy through coordinated modulation of multiple signaling pathways. MyD88- and Pik3r3- associated networks emerged as potential molecular mechanisms underlying BNP-mediated responses and may represent promising targets for future investigation.
CONCLUSION: This study provides transcriptomic evidence that BNP may attenuate cardiomyocyte hypertrophy and identifies MyD88- and Pik3r3-associated signaling networks as potential molecular mediators of this response. These findings suggest possible mechanisms underlying the protective effects of BNP and provide a foundation for future functional validation studies in hypertrophic heart disease.