Mitochondrial Dysfunction and Oxidative Stress in Cellular Autophagy, Senescence and Age-Related Disease

Aging is accompanied by progressive mitochondrial dysfunction and increased oxidative stress, both of which contribute to impaired cellular homeostasis. Mitochondria are not only the primary source of cellular energy but also major regulators of reactive oxygen species (ROS) and cell fate. Excessive ROS can damage mitochondrial DNA, proteins, and lipids, triggering cellular senescence and impairing autophagy. Autophagy—particularly mitophagy—plays a critical role in maintaining mitochondrial quality, but this process declines with age, leading to the accumulation of dysfunctional organelles and increased inflammation. Cellular senescence, further exacerbated by mitochondrial stress, contributes to tissue degeneration through the senescence-associated secretory phenotype (SASP). Understanding the interplay between mitochondrial dysfunction, oxidative stress, autophagy, and senescence is crucial for identifying therapeutic targets to delay aging and prevent age-related diseases. This special issue invites original research and reviews addressing these interconnected pathways and their roles in aging and pathology.

The goal of this special issue is to investigate the mechanistic roles of mitochondrial dysfunction and oxidative stress in regulating cellular autophagy and senescence, and to elucidate how these interconnected pathways contribute to the onset and progression of age-related diseases. By bringing together cutting-edge research and comprehensive reviews, this issue aims to provide new insights into mitochondrial biology, redox signaling, and cellular homeostasis, while identifying novel therapeutic targets and intervention strategies that could delay or reverse cellular aging and disease pathology.

This special issue aims to explore the complex and dynamic interplay between mitochondrial dysfunction, oxidative stress, and the regulation of cellular autophagy and senescence in the context of age-related diseases. Mitochondria serve as both a source and a target of reactive oxygen species (ROS), making them central to redox homeostasis, bioenergetics, and cell fate decisions. Dysregulation in these pathways is a hallmark of aging and is implicated in neurodegeneration, cancer, metabolic disorders, and cardiovascular disease. We welcome original research and reviews that address molecular mechanisms, signaling pathways, therapeutic targets, and novel biomarkers related to mitochondrial and redox biology in aging and disease.

Article types and fees

This Issue accepts the following article types, unless otherwise specified in the Issue description:

• Brief Communication
• Commentary
• Mini Review
• Original Research
• Review

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Issue accepts the following article types, unless otherwise specified in the Issue description:

• Brief Communication
• Commentary
• Mini Review
• Original Research
• Review

Keywords: Senescence, Autophagy, Cancer, resistance, Mitochondria, Cardiovascular, Neurodegenerative diseases, Oxidative stress