Related Experiment Video

Updated: Sep 10, 2025

A Murine Model of Hemodialysis Access-Related Hand Dysfunction
08:39

A Murine Model of Hemodialysis Access-Related Hand Dysfunction

Published on: May 31, 2022

1.8K

Angiotensin-(1-7) Mitigates Progression from Acute Kidney Injury to Chronic Kidney Disease Via Renin-Angiotensin

Minzi Qiu1, Yanxia Chen1, Siyue Huang1

  • 1Department of Nephrology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 1, Minde Road, Donghu District, Nanchang, 330006, Jiangxi Province, P.R. China.

Inflammation
|August 26, 2025
PubMed
Abstract

Insights

Angiotensin-(1-7) peptide shows promise in preventing acute kidney injury (AKI) from progressing to chronic kidney disease (CKD). This peptide therapy modulates the renin-angiotensin system (RAS), reducing fibrosis and inflammation in kidneys.

Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Pharmacology

Background:

  • Acute kidney injury (AKI) frequently advances to chronic kidney disease (CKD), posing a significant clinical challenge.
  • The renin-angiotensin system (RAS), particularly the protective Angiotensin-(1-7) (Ang-(1-7)) pathway, presents a therapeutic target for mitigating AKI progression.
  • This study investigates the renoprotective effects of Ang-(1-7) in a murine model of ischemia-reperfusion (I/R) injury-induced AKI.

Purpose of the Study:

  • To evaluate the therapeutic potential of Angiotensin-(1-7) (Ang-(1-7)) in preventing the progression of acute kidney injury (AKI) to chronic kidney disease (CKD).
  • To investigate the impact of Ang-(1-7) on key biomarkers of kidney injury, fibrosis, and inflammation in a murine I/R model.
  • To explore the modulation of the renin-angiotensin system (RAS) by Ang-(1-7) treatment in the context of AKI.

Main Methods:

  • Induction of bilateral renal ischemia-reperfusion (I/R) injury in adult male Balb/c mice to model AKI.
  • Administration of varying doses of Angiotensin-(1-7) (Ang-(1-7)) to treated mice.
  • Assessment of serum biomarkers (Angiotensin II, TGF-β1, SOD) using ELISA, renal fibrosis markers (Collagen I) via immunohistochemistry, and RAS pathway proteins (ACE2, AT1R) using Western blotting.

Main Results:

  • Angiotensin-(1-7) (Ang-(1-7)) treatment significantly reduced serum Angiotensin II (Ang II) and Transforming Growth Factor-β1 (TGF-β1) levels.
  • A dose-dependent increase in Superoxide Dismutase (SOD) was observed, indicating enhanced antioxidant capacity.
  • Ang-(1-7) administration markedly decreased renal fibrosis markers (Collagen I) and inflammatory cytokines, and modulated RAS components, increasing ACE2 and decreasing AT1R expression.

Conclusions:

  • Angiotensin-(1-7) (Ang-(1-7)) demonstrates significant potential in preventing the progression of acute kidney injury (AKI) to chronic kidney disease (CKD).
  • The renoprotective effects are attributed to the modulation of the renin-angiotensin system (RAS) towards a protective state, reducing fibrosis and inflammation.
  • These findings support further clinical investigation of Ang-(1-7) or Mas receptor agonists for managing kidney diseases.
Keywords:
Acute kidney injuryAngiotensin-(1–7)Chronic kidney diseaseInflammationRenal fibrosisRenin-angiotensin system

More Related Videos

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice02:45

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice

Published on: February 2, 2024

1.8K
A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

5.0K

Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
72
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
57
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
819
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...
505
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
72
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
875