Next Article in Journal
Identification of Retinopathy of Prematurity Related miRNAs in Hyperoxia-Induced Neonatal Rats by Deep Sequencing
Next Article in Special Issue
Nitric Oxide and Reactive Oxygen Species in the Pathogenesis of Preeclampsia
Previous Article in Journal
Nutritional Composition and Antioxidant Capacity in Edible Flowers: Characterisation of Phenolic Compounds by HPLC-DAD-ESI/MSn
Previous Article in Special Issue
Chlamydia pneumoniae and Oxidative Stress in Cardiovascular Disease: State of the Art and Prevention Strategies
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2015, 16(1), 823-839; doi:10.3390/ijms16010823

Pathogenesis of Target Organ Damage in Hypertension: Role of Mitochondrial Oxidative Stress

1
Department of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome 00189, Italy
2
Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Neuromed, Pozzilli 86077, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Francis J. Miller
Received: 18 November 2014 / Accepted: 26 December 2014 / Published: 31 December 2014
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Disease 2015)
View Full-Text   |   Download PDF [1201 KB, uploaded 31 December 2014]   |  

Abstract

Hypertension causes target organ damage (TOD) that involves vasculature, heart, brain and kidneys. Complex biochemical, hormonal and hemodynamic mechanisms are involved in the pathogenesis of TOD. Common to all these processes is an increased bioavailability of reactive oxygen species (ROS). Both in vitro and in vivo studies explored the role of mitochondrial oxidative stress as a mechanism involved in the pathogenesis of TOD in hypertension, especially focusing on atherosclerosis, heart disease, renal failure, cerebrovascular disease. Both dysfunction of mitochondrial proteins, such as uncoupling protein-2 (UCP2), superoxide dismutase (SOD) 2, peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), calcium channels, and the interaction between mitochondria and other sources of ROS, such as NADPH oxidase, play an important role in the development of endothelial dysfunction, cardiac hypertrophy, renal and cerebral damage in hypertension. Commonly used anti-hypertensive drugs have shown protective effects against mitochondrial-dependent oxidative stress. Notably, few mitochondrial proteins can be considered therapeutic targets on their own. In fact, antioxidant therapies specifically targeted at mitochondria represent promising strategies to reduce mitochondrial dysfunction and related hypertensive TOD. In the present article, we discuss the role of mitochondrial oxidative stress as a contributing factor to hypertensive TOD development. We also provide an overview of mitochondria-based treatment strategies that may reveal useful to prevent TOD and reduce its progression. View Full-Text
Keywords: target organ damage; hypertension; mitochondrial dysfunction; oxidative stress target organ damage; hypertension; mitochondrial dysfunction; oxidative stress
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Rubattu, S.; Pagliaro, B.; Pierelli, G.; Santolamazza, C.; Di Castro, S.; Mennuni, S.; Volpe, M. Pathogenesis of Target Organ Damage in Hypertension: Role of Mitochondrial Oxidative Stress. Int. J. Mol. Sci. 2015, 16, 823-839.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top