Utp14a, an essential component of a large ribonucleoprotein complex, is involved in ribosome biogenesis as it activates the RNA helicase DHX37 to facilitate maturation of the small ribosomal subunit [4]. It also plays roles in various cellular processes associated with different pathways and diseases, indicating its broad biological importance. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, could potentially be valuable for further studying its functions.

In obesity-induced cardiac injury, Utp14a was identified as a hub gene. Obesity-related pathological changes in the heart, like increased collagen fibers, decreased microvessels, and endothelial cell damage, may be associated with Utp14a's role in modulating cardiac angiogenesis [1].

In colorectal cancer, hUTP14a (human Utp14a) promotes angiogenesis by upregulating PDGFA expression. Knockdown of hUTP14a in CRC cells impairs tube formation and migration of endothelial cells, and in vivo depletion of hUTP14a decreases microvascular density in mouse xenografts [2].

In esophageal squamous cell carcinoma (ESCC), knockdown of Utp14A suppresses cell migration and proliferation, and high expression of Utp14a is associated with poor prognosis, suggesting its role in promoting ESCC progression [3,5].

In conclusion, Utp14a is crucial for ribosome biogenesis and significantly impacts processes like angiogenesis and tumor cell proliferation. Model-based research, especially KO/CKO mouse models as indicated in some studies, has revealed its role in diseases such as obesity-induced cardiac injury, colorectal cancer, and ESCC. Understanding Utp14a's functions provides insights into disease mechanisms and may offer potential therapeutic targets.