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et al., 2020)
doi: 10.1096/fj.01-0269fje 493 DengDYanJWuYWuKLiW
2013 PMC3781550 Conte, MS
Potential mechanisms range from changes in the extracellular matrix (myocardial fibrosis, inflammation) 79 to impaired calcium handling 80 or modification of sarcomeric proteins, 81 which have all been reviewed by others
doi: 10.1111/j.1749-6632.2002.tb04278.x
Although these acquired functional deficiencies generally produce less severe effects than genetic mutations, they can significantly disrupt metabolic homeostasis in susceptible individuals
