Related Experiment Video

Updated: Jul 26, 2025

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
08:21

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

Published on: October 26, 2020

4.9K

Signaling mechanisms in renal compensatory hypertrophy revealed by multi-omics

Hiroaki Kikuchi1, Chung-Lin Chou2, Chin-Rang Yang2

  • 1Epithelial Systems Biology Laboratory, Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. hiroaki.k1114@gmail.com.

Nature Communications
|June 16, 2023
PubMed

Insights

Losing a kidney triggers compensatory growth in the remaining one. Researchers found that peroxisome proliferator-activated receptor alpha (PPARα) is key to this kidney regrowth, specifically in proximal tubule cells.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genomics

Background:

  • Compensatory growth of the remaining kidney after nephrectomy is clinically significant.
  • The underlying molecular mechanisms driving renal compensatory hypertrophy remain largely unknown.

Purpose of the Study:

  • To identify signaling pathways involved in renal compensatory hypertrophy using a multi-omic approach.
  • To investigate the role of peroxisome proliferator-activated receptor alpha (PPARα) in this process.

Main Methods:

  • Unilateral nephrectomy model in male mice.
  • Multi-omic analysis (genomics, transcriptomics, proteomics, etc.).
  • Analysis of proximal tubule cell size and function.

Main Results:

  • Identified PPARα as a key signaling molecule in compensatory renal hypertrophy.
  • Demonstrated that PPARα influences proximal tubule cell size.
  • Established PPARα as a likely mediator of compensatory proximal tubule hypertrophy.

Conclusions:

  • PPARα is a critical regulator of proximal tubule cell adaptation following kidney loss.
  • Understanding PPARα's role may offer therapeutic targets for kidney disease.

More Related Videos

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

227
Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes11:47

Using 2-Photon Microscopy to Quantify the Effects of Chronic Unilateral Ureteral Obstruction on Glomerular Processes

Published on: March 4, 2022

2.3K

Related Concept Videos

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...
16
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
33.4K
Endocrine Signaling01:45

Endocrine Signaling

Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
64.5K
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
2.1K
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...
469
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...
1.7K