ZFP36 is an RNA-binding protein containing CCCH-type zinc finger motifs that regulates mRNA stability by binding to AU-rich elements in 3'-untranslated regions 1. Its primary function is post-transcriptional control of gene expression through mRNA decay mechanisms 1. Mechanistically, ZFP36 suppresses target mRNA stability and translation across multiple pathways. In hepatic stellate cells, ZFP36 destabilizes ATG16L1 mRNA to inhibit autophagy-dependent ferroptosis 2. In adipose tissue, ZFP36 represses RNF128 mRNA stability, thereby activating Sirt1 signaling to regulate lipid metabolism 3. In vascular smooth muscle, ZFP36 destabilizes RGS2 mRNA to enhance calcium signaling and blood pressure regulation 4. In prostate cancer, ZFP36 reduces CDK6 expression to suppress cell cycle progression 5. ZFP36 dysregulation is implicated in multiple diseases. Reduced ZFP36 expression correlates with prostate cancer progression and poor prognosis 5, and ZFP36 is identified as a potential biomarker in psoriasis, atherosclerosis, and chr19 kidney disease with NAFLD 67. ZFP36 downregulation in obesity contributes to metabolic dysfunction 3, while upregulation in hypertension promotes pathological vascular remodeling 4. Clinically, ZFP36 represents a therapeutic target: adipose ZFP36 overexpression protects against diet-induced obesity, ZFP36 inhibition in vascular tissue ameliorates hypertension, and ZFP36 restoration may suppress prostate cancer progression 345.