Ask about this productRelated genes to: DPP4 protein
- Gene:
- DPP4 NIH gene
- Name:
- dipeptidyl peptidase 4
- Previous symbol:
- CD26, ADCP2
- Synonyms:
- DPPIV
- Chromosome:
- 2q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-05
- Date modifiied:
- 2016-02-05
Related products to: DPP4 protein
Related articles to: DPP4 protein
- Adverse events (AEs) detected in tweets and in the FDA Adverse Event Reporting System (FAERS) provide valuable insights into patient experiences with oral hypoglycemic agents including sodium-glucose transporter 2 (SGLT2) and dipeptidyl peptidase-4 (DPP4) inhibitors. This study compared the side effects identified from tweets with those in the FAERS to identify the AEs associated with each drug. - Source: PubMed
Oh Se-HoonPark Dong-YoungSong Yun-Kyoung - Sitagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor used to treat type 2 diabetes. However, several studies have demonstrated its anti-inflammatory and immunomodulatory properties. The aim of this study was to investigate the effect of sitagliptin on the functional and phenotypic properties of human neutrophils under normal (NG, 5.5 mM)- and high (HG, 22 mM)-glucose conditions in vitro. Neutrophils were pretreated with varying concentrations of sitagliptin and stimulated with phorbol-12-myristate-13-acetate (PMA), N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), calcium ionophore (CaI), or opsonized zymosan (OpZym). Survival, phenotypic, and functional characteristics were then assessed. Our results showed that sitagliptin was non-cytotoxic to neutrophils even at very high concentrations. It decreased the production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs), generally following a stimulus- and concentration-dependent pattern. The effect was more pronounced under HG conditions. Furthermore, sitagliptin showed a significant ROS-scavenging effect in a cell-free system. It also rapidly altered the expression of surface markers in both resting and fMLP-stimulated neutrophils, typically upregulating CD10, CD16, CD62L, CD63, CD88, CD89, and PD-L1, and downregulating CD11b/CD18, CD66b, and CD182, a phenotype consistent with a dampened, less-primed activation state of these cells. In conclusion, sitagliptin exhibited marked antioxidative/ROS-scavenging activity in neutrophil cultures and induced a coordinated shift in neutrophil phenotype, accompanied by suppression of NETosis under both NG and HG conditions. Collectively, these data support the view that neutrophils may constitute an additional cellular target contributing to sitagliptin's anti-inflammatory and immunomodulatory profile. - Source: PubMed
Publication date: 2026/04/10
Mališ VanjaDrakul MarijaRakočević SaraKozić LjiljanaDubovina AnđelaPopović DarinkaBokonjić DejanMihajlović DušanČolić Miodrag - : Type 2 diabetes mellitus (DM) commonly coexists with heart failure (HF) and is associated with increased cardiovascular (CV) morbidity and mortality. Although dipeptidyl peptidase-4 (DPP-4) inhibitors are widely used for glycemic control, their CV safety in patients with established HF, particularly across HF phenotypes, remains uncertain. To evaluate the association between DPP-4 inhibitor use and 6-month CV mortality in patients with DM and HF, and to assess whether this association differs across HF phenotypes: HF with preserved ejection fraction (HFpEF), HF with mildly reduced ejection fraction (HFmrEF), HF with reduced ejection fraction (HFrEF). : We conducted a retrospective cohort study at King Abdulaziz Medical City from January 2017 to December 2024 that included adults with DM and echocardiographically confirmed HF. Patients receiving DPP-4 inhibitors were compared with non-users. The primary outcome was 6-month CV mortality. Propensity score overlap weighting targeting the average treatment effect in the overlap population was applied to balance baseline characteristics. Weighted logistic regression with interaction terms was used to assess effect modification by HF phenotype. : Among 3435 patients (median age 69 years; 51.3% female), 1921 (55.9%) received a DPP-4 inhibitor, predominantly sitagliptin. In unadjusted analyses, CV mortality was numerically lower among DPP-4 inhibitor users across HF phenotypes. However, after overlap weighting, CV mortality was similar between users and non-users within HFpEF (7.1% vs. 8.0%; OR 0.88, 95% CI 0.51-1.52; = 0.646), HFmrEF (2.6% vs. 5.0%; OR 0.50, 95% CI 0.09-2.86; = 0.436), and HFrEF (6.4% vs. 6.4%; OR 1.00, 95% CI 0.48-2.07; = 0.992). No significant interaction was observed between DPP-4 inhibitor use and HF phenotype (interaction > 0.05). : In this large real-world cohort of patients with DM and established HF, DPP-4 inhibitor use was not associated with increased or reduced 6-month CV mortality after robust adjustment. The neutral association was consistent across HF phenotypes, supporting the CV safety of DPP-4 inhibitors, predominantly sitagliptin, in contemporary HF management. - Source: PubMed
Publication date: 2026/04/21
Alfehaid LamaAlamer AhmadAlhantush AtheerYami Majed S Al - : The mechanism of action of genes related to lactate metabolism in papillary thyroid carcinoma (PTC) is still unclear. In this study, key genes that play a role in PTC were selected from the known genes related to lactate metabolism, and their roles in promoting lactate metabolism in PTC cells were investigated. : Through bioinformatics analysis and cell experiments, the roles of the relevant genes in lactate metabolism and their roles in the occurrence and development of PTC were verified. : Through bioinformatics analysis, 12 candidate genes were obtained. Through qRT-PCR experiments, it was confirmed that the expressions of and were higher in thyroid papillary carcinoma than in normal PTC cells. By inhibiting the expression of and using siRNA, the invasion and proliferation abilities of PTC could be reduced. Compared with normal thyroid cells, the contents of lactic acid and LDHA in PTC cells were higher. Knocking down the expression of and would reduce the lactate production ability of PTC cells, and and promoted the accumulation of lactate in PTC cells.: In this study, by screening the differentially expressed lactate metabolism genes in PTC, different prognostic subtypes were constructed based on the molecular expression patterns. Multi-group student's t-tests were conducted on the differential signaling pathways and tumor immune regulation of the prognostic subtypes, and a PTC prognosis prediction model was constructed. It was further confirmed that the lactate metabolism genes and are highly expressed in PTC and can regulate the proliferation, invasion, metastasis and lactate metabolism of PTC cells. - Source: PubMed
Publication date: 2026/04/16
Mu ShiJiXue JinXia FadaOuyang XiwuFu GuodeGui RuotongWang HaihongBai Ning - Despite major advances in glucose-lowering therapies, a substantial proportion of individuals with type 2 diabetes (T2DM) do not achieve recommended glycemic targets, maintaining a high risk of microvascular and macrovascular complications. While current guidelines prioritize agents with proven cardiovascular and renal benefits (treat-to-benefit), optimal glycemic control (treat-to-target) remains a cornerstone of diabetes management. This review supports an integrated therapeutic framework in which both strategies are pursued in parallel and examines the role of dipeptidyl peptidase-4 inhibitors (DPP-4is) within this context. DPP-4is provide clinically meaningful HbA1c reductions, approximately 0.6-1.1%, with a low risk of hypoglycemia, weight neutrality, and a favorable tolerability profile. Cardiovascular outcome trials have established their cardiovascular safety, and they are particularly suitable as add-on treatment to metformin, SGLT-2 inhibitors, or insulin, enabling safe intensification to achieve glycemic targets while maintaining cardiorenal-protective regimens. DPP-4is tolerability makes them specifically indicated for older patients. In contemporary diabetes care, DPP-4is-particularly sitagliptin-remain a versatile option bridging treat-to-target and treat-to-benefit paradigms to support comprehensive cardiovascular-kidney-metabolic (CKM) reduction in T2DM. - Source: PubMed
Publication date: 2026/05/01
Avogaro AngeloFiaccadori EnricoRizzo Maria Rosaria