Related Experiment Video

Updated: May 18, 2026

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

Dipeptidyl peptidase-4 modulates left ventricular dysfunction in chronic heart failure via angiogenesis-dependent and

Toshimasa Shigeta1, Morihiko Aoyama, Yasuko K Bando

  • 1Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Circulation
|October 5, 2012
PubMed

Insights

Dipeptidyl peptidase-4 (DPP4) inhibition reverses diastolic heart failure (DHF) by improving blood vessel function and heart contractility. Circulating DPP4 levels may serve as a biomarker for monitoring DHF.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Biochemistry

Background:

  • Dipeptidyl peptidase-4 (DPP4) inhibition benefits acute myocardial ischemia.
  • The role of DPP4 in chronic heart failure (CHF) without coronary artery disease is not well understood.

Purpose of the Study:

  • To investigate the role of DPP4 in diastolic left ventricular dysfunction (DHF).
  • To explore DPP4 inhibition as a therapeutic strategy for DHF.

Main Methods:

  • Localized membrane-bound DPP4 in rat and human heart capillaries.
  • Investigated DPP4 activation in diabetic rats and pressure-overloaded rats.
  • Assessed circulating DPP4 activity in patients with DHF.

Main Results:

  • Diabetes mellitus activates DPP4, reducing angiogenesis and causing DHF with fibrosis via MMP-2/TIMP-2 ratio.
  • DPP4 suppression reversed diabetic DHF and microvasculopathy.
  • DPP4 inhibition reversed pressure-overload-induced DHF through a GLP-1/cAMP pathway.
  • Circulating DPP4 activity in DHF patients correlated with coronary sinus activity and echocardiographic parameters.

Conclusions:

  • DPP4 inhibition reverses DHF via local and systemic mechanisms.
  • DPP4 inhibition impacts angiogenesis and cardiac contractility.
  • Circulating DPP4 may be a potential biomarker for monitoring DHF.
Abstract

More Related Videos

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats07:41

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Published on: March 1, 2022

Related Concept Videos

Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...