Oxidative Stress Modulation in Cancer and Diabetes

Oxidative stress results from an imbalance between the generation of reactive oxygen species and the capacity of endogenous antioxidant systems. In cancer, elevated oxidative stress can promote oncogenic transformation, DNA damage and tumour progression, yet cancer cells may also exploit antioxidant pathways to survive chemotherapy. In diabetes, chronic hyperglycaemia drives overproduction of reactive species, leading to β-cell dysfunction, vascular complications and organ damage. Modulation of oxidative stress therefore presents a dual therapeutic challenge: to exacerbate redox imbalance in malignant cells while restoring redox homeostasis in diabetic tissues. Recent research has elucidated how naturally occurring phenolic acids and targeted inhibitors can recalibrate redox signalling, influence mitochondrial function, and regulate key survival pathways such as mTOR/AKT, with implications for novel adjuvant treatments in both diseases.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Oxidative Stress Modulation in Cancer and Diabetes publication trend

The graph below shows the total number of articles in oxidative stress modulation in cancer and diabetes across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive Oxygen Species (ROS): Chemically reactive molecules containing oxygen, such as superoxide and hydrogen peroxide, which can damage cellular components.

Antioxidant Enzyme: Proteins such as superoxide dismutase and catalase that catalyse the removal of reactive oxygen species to maintain redox balance.

Apoptosis: Programmed cell death characterised by caspase activation, DNA fragmentation and membrane blebbing, crucial for eliminating damaged or unwanted cells.

Autophagy: A regulated process for the degradation and recycling of cellular components through lysosomal pathways, often activated in response to stress.

Mitochondrial Biogenesis: The process by which cells increase mitochondrial mass and copy number, regulated by factors including PGC-1α and NRF-1, to meet energy and biosynthetic demands.

mTOR/AKT Signalling Pathway: A central intracellular cascade that integrates nutrient and growth factor signals to regulate cell growth, survival and metabolism; commonly activated in cancer.

References

1. Effects of Syringic Acid on Apoptosis, Inflammation, and AKT/mTOR Signaling Pathway in Gastric Cancer Cells. Frontiers in Nutrition (2021).
2. Neuroprotective Effect of Syringic Acid by Modulation of Oxidative Stress and Mitochondrial Mass in Diabetic Rats. BioMed Research International (2020).
3. Syringic Acid Ameliorates Cardiac, Hepatic, Renal and Neuronal Damage Induced by Chronic Hyperglycaemia in Wistar Rats: A Behavioural, Biochemical and Histological Analysis. Molecules (2022).