SCIENCE

Mitochondria

Mitochondria

Mitochondria

Mitochondria are organelles that act as energy factories of our cells and play a key role in the energy metabolism. Mitochondria consume oxygen to convert nutrients such as carbohydrates and fats into chemical energy sources (adenosine triphosphate - ATP) for cells, while simultaneously producing free radicals (reactive oxygen species - ROS) as byproducts. In a healthy state, mitochondria produce plenty of ATP without much ROS, or damaged parts of mitochondria by ROS are recycled to create newly functional mitochondria.

Mitochondrial Dysfunction in Diseases

Mitochondrial dysfunction may occur due to various factors such as aging, nutritional imbalance, and hereditary causes. Dysfunctional mitochondria are incapable of producing sufficient ATP and generate excess free radicals, which induce cellular oxidative stress. This in turns activates inflammatory signaling pathways, causes protein damage, and leads to overall cellular dysfunction. Mitochondrial dysfunction is reported to underlie various diseases: obesity, type 2 diabetes (T2D), nonalcoholic steatohepatitis (NASH), neurodegenerative diseases, age-related macular degeneration (AMD), diabetic retinopathy, and others.

  • Obesity
  • NAFLD
  • Dyslipidemia
  • Hypertension
  • Diabetes
  • Neurodegenerative
    Disease
  • Inflammatory Disease
  • Retinal Disease

Mitochondrial Dysfunction in Diseases

  • Obesity
  • NAFLD
  • Dyslipidemia
  • Hypertension
  • Diabetes
  • Neurodegenerative
    Disease
  • Inflammatory
    Disease
  • Retinal Disease

Mitochondrial Dysfunction in Diseases

Mitochondrial dysfunction may occur due to various factors such as aging, nutritional imbalance, and hereditary causes. Dysfunctional mitochondria are incapable of producing sufficient ATP and generate excess free radicals, which induce cellular oxidative stress. This in turns activates inflammatory signaling pathways, causes protein damage, and leads to overall cellular dysfunction. Mitochondrial dysfunction is reported to underlie various diseases: obesity, type 2 diabetes (T2D), nonalcoholic steatohepatitis (NASH), neurodegenerative diseases, age-related macular degeneration (AMD), diabetic retinopathy, and others.

Paraoxonase (PON)

Paraoxonase (PON)

Paraoxonase (PON) family consists of three proteins (PON1, PON2, and PON3). Their main reported function is antioxidant activity. PON1 and PON3 are mainly present in HDL in blood, and PON1 plays part in removing oxidized-LDL. PON2 is a membrane-bound protein and is located in the membrane of endoplasmic reticulum and mitochondria. PON2 is reported to play part in reducing ROS levels, thereby protecting cells from oxidative stress and inflammation. Glaceum’s compounds HSG4112 and HGR4113 target this PON family proteins.

Improving Mitochondrial Function

Improving Mitochondrial Function

The main function of HSG4112 and HGR4113 is to improve the mitochondrial function via PON2 protein, by reducing ROS levels and eventually ameliorating oxidative stress and inflammation. Glaceum additionally discovered that both HSG4112 and HGR4113 induce mitophagy, which is the specific recycling of mitochondria, and autophagy, which is the recycling of overall damaged organelles, via PON2. These effects result in normalization of mitochondria and the cellular energy metabolism. HSG4112 and HGR4113 also have an additional function of removing oxidized LDL from the blood via PON1.