Key result
Endogenous molecules inactivated during cardiac hypertrophy act as a natural defense against its development.
Why the study?
The mechanisms by which endogenous molecules inhibit the occurrence and development of pathological cardiac hypertrophy are not fully characterized.
This review highlights a class of endogenous molecules that inhibit pathological cardiac hypertrophy, serving as a natural first line of defense.
Embryonic reprogramming may identify hypertrophy targets; leaves open clinical validation of metabolic or MHC modulation.
The embryonic phenotype transformation of cardiomyocytes is an important characteristic of pathological cardiac hypertrophy. It includes transcriptional reprogramming of gene expression, a switch from lipid metabolism to carbohydrate metabolism, and a shift from α-myosin heavy chain (MHC) to fetal ß-MHC expression. The embryonic and adult cardiacmyocytes have distinct gene expression profiles. A series of genes that are expressed in embryos are later shut down after birth through the inhibition of endogenous constitutively activated molecules. These genes can be reactivated if these inhibitors are inactivated or down regulated, as occurs under certain pathological conditions. This promotes pathological cardiac hypertrophy. In this review, we list a class of endogenous molecules whose expression is inactivated during cardiac hypertrophy. They play a positive role in inhibition of the occurrence and development of cardiac hypertrophy and constitute the first natural line of defense against pathological cardiac hypertrophy.
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Fan et al. (2013) conducted a review in Cardiac hypertrophy. Endogenous molecules was evaluated. Endogenous molecules whose expression is inactivated during cardiac hypertrophy play a positive role in inhibiting its development, constituting a natural line of defense.
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