Mitochondrial Dysfunction in Pulmonary Hypertension.
Gusty Rizky Teguh RyantoRatoe SurayaTatsuya NaganoPublished in: Antioxidants (Basel, Switzerland) (2023)
Pulmonary hypertension (PH) is a multi-etiological condition with a similar hemodynamic clinical sign and end result of right heart failure. Although its causes vary, a similar link across all the classifications is the presence of mitochondrial dysfunction. Mitochondria, as the powerhouse of the cells, hold a number of vital roles in maintaining normal cellular homeostasis, including the pulmonary vascular cells. As such, any disturbance in the normal functions of mitochondria could lead to major pathological consequences. The Warburg effect has been established as a major finding in PH conditions, but other mitochondria-related metabolic and oxidative stress factors have also been reported, making important contributions to the progression of pulmonary vascular remodeling that is commonly found in PH pathophysiology. In this review, we will discuss the role of the mitochondria in maintaining a normal vasculature, how it could be altered during pulmonary vascular remodeling, and the therapeutic options available that can treat its dysfunction.
Keyphrases
- pulmonary hypertension
- induced apoptosis
- oxidative stress
- pulmonary artery
- cell death
- cell cycle arrest
- heart failure
- pulmonary arterial hypertension
- reactive oxygen species
- endoplasmic reticulum
- endoplasmic reticulum stress
- dna damage
- signaling pathway
- left ventricular
- ischemia reperfusion injury
- coronary artery
- drug induced