Human Genome Organization–Symbolized Muscle-Enriched A-Type Lamin-Interacting Protein to Clear Up Confusion

Abstract

To the Editor: We were surprised to read the recent study published in Circulation Research by Huang et al1 entitled “CIP, a Cardiac Isl1-Interacting Protein, Represses Cardiomyocyte Hypertrophy” as it simply validated much of our published work on the discovery and initial biological characterization of muscle-enriched A-type lamin-interacting protein (MLIP).2,3 Huang et al1 have reaffirmed our findings and provided limited new information as to the putative biological role of MLIP. Laminopathies are tissue-specific, degenerative diseases associated with nuclear envelope proteins, with lamin A/C and emerin being the best-characterized examples known to date.4 Clinical symptoms are varied and include cardiovascular defects (dilated cardiomyopathy and atherosclerosis), muscular dystrophy (muscle wasting), lipodystrophy (fat wasting), diabetes mellitus, neuropathy, and progeria (premature aging).4–6 All these conditions are life-threatening and, with only limited palliative treatment available, many patients die in childhood or early adulthood. A major focus of current research is to determine the paradox of how primary genetic defects in …