Cardiac proliferation

Cardiac proliferation refers to the ability of cardiomyocytes to progress through the cell cycle and divide, driving heart growth during embryonic development and early postnatal stages in mammals[5][1][2]. In adult mammals, cardiomyocytes typically exit the cell cycle and do not significantly proliferate, limiting the heart’s ability to regenerate after injury. Multiple signaling pathways—including Notch, Wnt/β-catenin, Hippo/Yap, IGF, and neuregulin—regulate cardiomyocyte proliferation, and modulation of these pathways is under investigation as a therapeutic avenue to stimulate cardiac regeneration in settings such as myocardial infarction[2][4][8]. Recent research focuses on methods to reactivate this proliferative capacity to promote recovery from heart injury[5][1]. Key context: - Cardiac proliferation describes a complex, multigenic process and is *not* a discrete molecular drug target such as a receptor, enzyme, or transporter[2][5]. - Instead, therapeutic efforts often focus on nodes within the signaling pathways that regulate this process (e.g., Yap, β-catenin, Notch1), which *are* canonical targets[2][4]. - Biomarkers such as Ki67 and phospho-Histone H3 are used to assess cardiomyocyte proliferation in experimental settings[7]. - Safety concerns around inducing cardiac proliferation include the risk of cancer (if uncontrolled) and the potential for disorganized tissue growth or arrhythmias[3][7]. There is something “wrong” with this target entry: “Cardiac proliferation” itself is not a canonical molecule, gene, or druggable target, but a physiological process influenced by many molecular players[2][5][3]. If you intended to focus on a specific molecule within cardiac proliferation (such as “Hippo pathway” or “YAP”), a more precise target name should be selected.

Other names

Cardiomyocyte proliferationCardiac myocyte proliferationHeart muscle cell proliferation