Larp7, or La ribonucleoprotein domain family member 7, is a master regulator involved in multiple crucial biological functions. It binds to 7SK RNA as part of the 7SK small nuclear ribonucleoprotein, inhibiting RNA polymerase II transcriptional activity. It also plays roles in RNP assembly, RNA modification, processing, and cellular transport [3]. Larp7 is associated with pathways like the DNA damage response and is vital for processes such as mitochondrial biogenesis, energy production, and maintaining normal cellular function [1]. Genetic models, especially KO and CKO mouse models, have been instrumental in studying its functions.

Global and cardiac-specific Larp7 knockout mice have demonstrated its significance in heart function. Constitutive Larp7 knockout in mice led to impaired mitochondrial biogenesis, myocardial hypoplasia, and mid-gestational lethality. Cardiac-specific inactivation resulted in defective mitochondrial biogenesis, impaired oxidative phosphorylation, elevated oxidative stress, and heart failure by 4 months of age. These defects were linked to reduced SIRT1 stability and deacetylase activity, affecting genes for oxidative phosphorylation and energy metabolism [1]. Deletion of Larp7 in a rodent model also led to senescent cell accumulation and premature aging, revealing its role in cellular senescence [2].

In conclusion, Larp7 is essential for mitochondrial biogenesis, energy production, and cardiac function. Mouse KO/CKO models have revealed its critical role in heart failure pathogenesis, cellular senescence, and related disease areas such as atherosclerosis. Understanding Larp7's functions through these models provides potential targets for therapeutic intervention in heart-related and age-related diseases.