Dpp3, also known as dipeptidyl peptidase 3, is the first zinc-dependent peptidase among DPPs. It has a unique HEXXGH catalytic sequence and is mainly located in the cytoplasm, associated with the degradation of oligopeptides with 4-10 amino acid residues. It participates in multiple cellular activities and pathophysiological mechanisms, including interacting with the renin-angiotensin system to regulate blood pressure, and is involved in pain signaling, inflammation, and oxidative stress [1].

In cardiovascular diseases, Dpp3 is used as a biomarker for poor prognosis in patients. For example, in cardiogenic shock patients, the plasma concentration of Dpp3 is closely related to mortality, and higher levels in ventilated patients may predict disease progression [1,6]. In cancer, Dpp3 is upregulated in breast, esophageal, and colorectal cancers. In breast cancer, it promotes tumorigenesis by stabilizing FASN and promoting lipid synthesis [2]. In esophageal carcinoma, its depletion reduces cell proliferation, migration, and tumor growth in a xenograft model [3]. In colorectal cancer, downregulation of Dpp3 inhibits cell proliferation, migration, and promotes apoptosis, and Dpp3 may act through targeting CDK1 [4]. In esophageal squamous cell carcinoma, knockdown of Dpp3 leads to reduced proliferation, increased apoptosis, and inhibited migration, along with down-regulation of the NRF2 pathway and increased sensitivity to oxidative stress and chemotherapy [5].

In conclusion, Dpp3 plays a significant role in cardiovascular diseases as a biomarker and potentially as a therapeutic target. In cancer, it promotes tumor development and progression in multiple types of malignancies. The study of Dpp3 in gene-knockout or conditional-knockout models, although not directly mentioned in the references in terms of these models, would further clarify its exact mechanisms in these biological processes and diseases, providing a better understanding of its biological functions and potential for treatment strategies.