2026-10-13T18:25:58Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33477136 2026-09-30T08:39:56Z category_24463 item_type_1 month_year_09_2026

Figure S1: Proteomic changes in treated Myh-GRK2 KO mice Michele Ciccarelli (425329) Cardiology (incl. cardiovascular diseases) ionizing radiation mithochondrial dysfunction GRK2 <p dir="ltr">Background: Radiation-induced heart disease (RIHD) is a complication of radiotherapy, caused by mitochondrial dysfunction and oxidative stress. G protein-coupled receptor kinase 2 (GRK2), beyond its typical role in G protein-coupled receptors (GPCRs) desensitization, has been linked to mitochondrial dynamics and cardiomyocyte health. Methods: We studied the effects of IR exposure in cardiomyocyte-specific GRK2 knockout (Myh-GRK2 KO) mice compared to GRK2 fl/fl (CTR) at 3h and 24h post-IR. GRK2 deficiency worsens IR-induced cardiac dysfunction at 3h post-exposure, persisting at 24h. Results: Proteomic analysis showed that GRK2 deficiency impairs the expression of mitochondrial proteins basally. TEM showed a reduction in mitochondrial number, increased swelling, and an altered structure in Myh-GRK2 KO mice. Importantly, GRK2 deficiency impaired activation of the PINK1/Parkin/DRP1 mitophagy axis, while increasing LC3 and decreasing p62 levels. In CTR mice, GRK2 moved to mitochondria post-IR, supporting mitochondrial integrity. Conclusion: GRK2 is essential for mitochondrial integrity during IR stress; its absence induces mitochondrial alterations, impairs mitophagy, and leads to cardiac dysfunction, identifying GRK2 as a therapeutic target.</p> 2026-09-30T08:39:56Z Image Figure 10.6084/m9.figshare.33477136.v1 https://figshare.com/articles/figure/Figure_S1_Proteomic_changes_in_treated_Myh-GRK2_KO_mice/33477136 CC BY 4.0