Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease.
Karina-Alexandra CojocaruIonut LuchianAncuta GoriucLucian-Mihai AntociCristian-Gabriel CiobanuRoxana PopescuCristiana-Elena VladMihaela BlajLiliana Georgeta FoiaPublished in: Antioxidants (Basel, Switzerland) (2023)
Mitochondria are subcellular organelles involved in essential cellular functions, including cytosolic calcium regulation, cell apoptosis, and reactive oxygen species production. They are the site of important biochemical pathways, including the tricarboxylic acid cycle, parts of the ureagenesis cycle, or haem synthesis. Mitochondria are responsible for the majority of cellular ATP production through OXPHOS. Mitochondrial dysfunction has been associated with metabolic pathologies such as diabetes, obesity, hypertension, neurodegenerative diseases, cellular aging, and cancer. In this article, we describe the pathophysiological changes in, and mitochondrial role of, metabolic disorders (diabetes, obesity, and cardiovascular disease) and their correlation with oxidative stress. We highlight the genetic changes identified at the mtDNA level. Additionally, we selected several representative biomarkers involved in oxidative stress and summarize the progress of therapeutic strategies.
Keyphrases
- cardiovascular disease
- oxidative stress
- type diabetes
- reactive oxygen species
- insulin resistance
- metabolic syndrome
- weight loss
- glycemic control
- high fat diet induced
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- weight gain
- diabetic rats
- blood pressure
- cell death
- cardiovascular events
- copy number
- cardiovascular risk factors
- papillary thyroid
- mitochondrial dna
- endoplasmic reticulum
- adipose tissue
- heat stress
- lymph node metastasis