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Article Abstract
CryAB, known as Alpha-B Crystallin, has also been shown to bind and increase the unfolding force of the filamentous protein. Mutation of CryAB at R120G causes serious cardiomyopathy but lacks ideal therapeutic drugs. In the present study, we constructed CryAB (R120G)-transgenic (TG) mice. One hundred and four differentially expressed genes (DEGs) in heart tissues of TG mice were screened through RNA sequencing. Gene ontology (GO) and KEGG pathway analyses highlighted enrichment in critical biological processes such as blood circulation regulation, contractile fiber formation, actin binding, thyroid hormone signaling, endocytosis, and alanine, aspartate, and glutamate metabolism. Protein-protein interaction (PPI) analysis pinpointed key hub genes, including DHTKD1, NKTR, SCN5A, CLCN1, RPA1, ACSF2, ACACB, TTC28, HSPA1B. By using Connectivity Map (CMap) analysis and transcriptome data, we identified phosphodiesterase (PDE) family as potential targets and several potential therapeutic candidates, with nortriptyline, torin-1, and cilostazol emerging as top candidates. Molecular docking simulations showed that Nortriptyline exhibited strong binding affinities with hub proteins, particularly SCN5A. These findings suggest promising new therapeutic strategies for CryAB(R120G)-related cardiomyopathy by targeting specific pathways and hub genes to mitigate cardiac dysfunction.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12398125 | PMC |
| http://dx.doi.org/10.1186/s12872-025-04897-0 | DOI Listing |
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