REFERENCES

1. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: an expanding universe. Cell 2023;186:243-78.

2. Kronenberg A. Radiation-induced genomic instability. Int J Radiat Biol 1994;66:603-9.

3. Aguilera A, García-Muse T. Causes of genome instability. Annu Rev Genet 2013;47:1-32.

4. Lindahl T. Instability and decay of the primary structure of DNA. Nature 1993;362:709-15.

5. Vilenchik MM, Knudson AG. Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer. Proc Natl Acad Sci U S A 2003;100:12871-6.

6. Cannan WJ, Pederson DS. Mechanisms and consequences of double-strand dna break formation in chromatin. J Cell Physiol 2016;231:3-14.

7. Chapman JR, Taylor MR, Boulton SJ. Playing the end game: DNA double-strand break repair pathway choice. Mol Cell 2012;47:497-510.

8. Haber JE. Deciphering the DNA damage response. Cell 2015;162:1183-5.

9. Ablasser A, Chen ZJ. cGAS in action: expanding roles in immunity and inflammation. Science 2019;363:eaat8657.

10. Motwani M, Pesiridis S, Fitzgerald KA. DNA sensing by the cGAS-STING pathway in health and disease. Nat Rev Genet 2019;20:657-74.

11. Rouhi L, Auguste G, Zhou Q, et al. Deletion of the Lmna gene in fibroblasts causes senescence-associated dilated cardiomyopathy by activating the double-stranded DNA damage response and induction of senescence-associated secretory phenotype. J Cardiovasc Aging 2022;2:30.

12. Rouhi L, Cheedipudi SM, Chen SN, et al. Haploinsufficiency of Tmem43 in cardiac myocytes activates the DNA damage response pathway leading to a late-onset senescence-associated pro-fibrotic cardiomyopathy. Cardiovasc Res 2021;117:2377-94.

13. Chen SN, Lombardi R, Karmouch J, et al. DNA damage response/TP53 pathway Is activated and contributes to the pathogenesis of dilated cardiomyopathy associated with LMNA (Lamin A/C) mutations. Circ Res 2019;124:856-73.

14. Marian AJ. Non-syndromic cardiac progeria in a patient with the rare pathogenic p.Asp300Asn variant in the LMNA gene. BMC Med Genet 2017;18:116.

15. Cheedipudi SM, Asghar S, Marian AJ. Genetic ablation of the DNA damage response pathway attenuates lamin-associated dilated cardiomyopathy in mice. JACC Basic Transl Sci 2022;7:1232-45.

16. Rouhi L, Fan S, Cheedipudi SM, et al. The EP300/TP53 pathway, a suppressor of the hippo and canonical WNT pathways, is activated in human hearts with arrhythmogenic cardiomyopathy in the absence of overt heart failure. Cardiovasc Res 2022;118:1466-78.

17. Collins AR. The comet assay for DNA damage and repair: principles, applications, and limitations. Mol Biotechnol 2004;26:249-61.

18. Cheedipudi SM, Matkovich SJ, Coarfa C, et al. Genomic reorganization of lamin-associated domains in cardiac myocytes is associated with differential gene expression and DNA methylation in human dilated cardiomyopathy. Circ Res 2019;124:1198-213.

19. Thyagarajan B, Guimarães MJ, Groth AC, Calos MP. Mammalian genomes contain active recombinase recognition sites. Gene 2000;244:47-54.

20. Loonstra A, Vooijs M, Beverloo HB, et al. Growth inhibition and DNA damage induced by Cre recombinase in mammalian cells. Proc Natl Acad Sci U S A 2001;98:9209-14.

21. Litviňuková M, Talavera-López C, Maatz H, et al. Cells of the adult human heart. Nature 2020;588:466-72.

22. Cordero-Reyes AM, Youker K, Hamilton DJ, Torre-Amione G, Marian AJ, Nagueh SF. Molecular, cellular, and functional characterization of myocardial regions in hypertrophic cardiomyopathy. Circ Cardiovasc Imaging 2012;5:419-22.

23. Hopfner KP, Hornung V. Molecular mechanisms and cellular functions of cGAS-STING signalling. Nat Rev Mol Cell Biol 2020;21:501-21.