Grsf1, also known as Guanine-rich RNA sequence binding factor 1, belongs to the heterogeneous nuclear ribonucleoproteins F/H (hnRNP F/H) subfamily. It is a mitochondrial RNA-binding protein involved in multiple biological processes. It plays a role in post-transcriptional regulation of genes, such as modulating mRNA stability, and is associated with pathways related to blood coagulation, cell senescence, and mitochondrial function [1,2,3,4,5]. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its functions.

In KO/CKO mouse models, Grsf1 deficiency leads to various phenotypes. In skeletal muscle, Grsf1-specific ablation in mice results in reduced muscle endurance in aged mice, with changes in mRNAs related to mitochondrial function, inflammation, and ion transport [4]. In ovarian granulosa cells, diminished Grsf1 expression exacerbates mitochondrial dysfunction, increases reactive oxygen species, and impairs ATP production [3]. In contrast, overexpression of Grsf1 in old mice liver decreases fibrinogen plasma level, reduces hypercoagulability, and mitigates blood coagulation activity, while knockdown in young mice liver has the opposite effects, indicating its role in regulating blood coagulation [1].

In conclusion, Grsf1 is crucial for maintaining mitochondrial function, suppressing cell senescence, and regulating blood coagulation. Studies using KO/CKO mouse models have revealed its significance in age-related conditions such as hypercoagulability, muscle functional decline, and ovarian aging, providing insights into potential therapeutic targets for these age-associated diseases.