Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

1.7K
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
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

473
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...
473
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

433
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
433
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

14.6K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
14.6K
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

26
Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
26
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

18
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...
18

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Trends in Nephrology: from treating kidney disease to maintaining kidney health.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2026
Same author

Environmental footprint of peritoneal dialysis in Europe: a comparative life cycle assessment across four European centres.

Clinical kidney journal·2026
Same author

Sex, menopause and chronic kidney disease in primary care.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2026
Same author

ATTR: the forgotten kidney amyloidosis.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2026
Same author

Optimization of artificial intelligence models for prediction of new-onset cardiovascular disease in patients with arterial hypertension.

PLOS digital health·2026
Same author

Prevalence of Hyperkalemia in a Contemporary European Cohort According to EKFC eGFR Categories.

Diagnostics (Basel, Switzerland)·2026

Related Experiment Video

Updated: Jul 30, 2025

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

11.8K

Mitochondrial Dysfunction in the Cardio-Renal Axis.

Nerea Mendez-Barbero1,2, Jorge Oller1,2, Ana B Sanz3,4

  • 1Laboratory of Vascular Pathology, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.

International Journal of Molecular Sciences
|May 13, 2023
PubMed
Summary
This summary is machine-generated.

Cardiovascular disease and chronic kidney disease together, known as cardio-renal syndrome, significantly increase mortality. Mitochondrial dysfunction is key, suggesting therapies targeting mitochondrial homeostasis could treat this condition.

Keywords:
cardiovascular diseasekidney diseasemitochondrial dysfunctionoxidative stresstreatment

More Related Videos

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

881
Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
08:19

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

2.5K

Related Experiment Videos

Last Updated: Jul 30, 2025

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

11.8K
Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

881
Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
08:19

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

2.5K

Area of Science:

  • Mitochondrial biology
  • Cardiovascular medicine
  • Nephrology

Background:

  • Cardiovascular disease (CVD) often complicates chronic kidney disease (CKD), leading to cardio-renal syndrome (CRS).
  • Patients with both conditions face a 20% to 500% increased risk of all-cause mortality.
  • Mitochondrial dysfunction is implicated in both cardiovascular and renal pathologies.

Purpose of the Study:

  • To review the role of mitochondrial homeostasis malfunction in CRS.
  • To explore how mitochondrial dysfunction contributes to vascular pathologies in CKD and vice versa.
  • To guide the development of novel therapeutic strategies for CRS.

Main Methods:

  • Literature review of preclinical studies.
  • Analysis of mitochondrial homeostasis pathways: biogenesis, dynamics, oxidative stress, and mitophagy.
  • Examination of the interplay between kidney injury and vascular pathologies.

Main Results:

  • Mitochondrial dysfunction is a central mechanism in CRS development and progression.
  • Impaired mitochondrial biogenesis, dynamics, oxidative stress, and mitophagy contribute to vascular damage.
  • Understanding these mechanisms offers insights into therapeutic interventions.

Conclusions:

  • Maintaining mitochondrial homeostasis is a promising therapeutic strategy for CRS.
  • Targeting mitochondrial pathways may mitigate the adverse effects of cardio-renal interactions.
  • Further research into mitochondrial mechanisms can inform novel CRS treatments.