Dose rectification of an imbalance between DPP4 and GLP-1 ameliorates chronic stress-related vascular aging and atherosclerosis?
Xian Wu ChengMegumi NarisawaEnze JinChenglin YuWenhu XuLimei PiaoPublished in: Clinical and experimental pharmacology & physiology (2018)
Exposure to psychosocial stress is a risk factor for cardiovascular disease, including vascular aging and regeneration. Dipeptidyl peptidase-4 (DPP-4) exerts many physiological and pharmacological functions by regulating its extremely abundant substrates [eg., glucagon-like peptide-1 (GLP-1), stromal cell-derived factor-1α/C-X-C chemokine receptor type-4, etc.]. Over the past decade, emerging data has revealed unexpected roles for DPP-4 and GLP-1 in intracellular signaling, oxidative stress production, lipid metabolism, cell apoptosis, immune activation, insulin resistance, and inflammation. This mini review focuses on recent findings in this field, highlighting an imbalance between DPP4 and GLP-1 as a potential therapeutic target in the management of vascular aging and atherosclerosis in animals under experimental stress conditions.
Keyphrases
- cardiovascular disease
- oxidative stress
- insulin resistance
- stem cells
- type diabetes
- stress induced
- metabolic syndrome
- adipose tissue
- mental health
- dna damage
- electronic health record
- big data
- mouse model
- fatty acid
- cardiovascular risk factors
- induced apoptosis
- binding protein
- human health
- coronary artery disease
- reactive oxygen species
- weight loss
- endoplasmic reticulum stress
- deep learning
- climate change