Population aging refers to an increase in the median age of a population, which is mainly caused by declining fertility rates and increasing longevity. In 2015, the population aged 60 years and older was 900 million worldwide, of which the number is predicted to reach almost 2 billion by 2050. Population aging has become a global problem. As well as the increased financial pressure on old-age support systems, the incidence of age-related diseases including stroke, chronic lung diseases, cardiovascular disease, and osteoarthritis is significantly rising. In addition, the elderly are more vulnerable to infection and at more risk of developing cancer. Senescence, on the cellular level, is an antagonistic response to the aging process that limits the proliferation of aged or damaged cells characterized by permanent growth arrest. The role of senescence in age-related diseases has been scrutinized by numerous studies involving both beneficial and deleterious effects, such as maintenance of the structure and the function of tissues following injury in the former, and induction of proinflammatory conditions and limiting tissue generation in the latter. Autophagy is a process that involves a series of highly regulated cellular activities to deliver cytoplasmic materials to lysosomes for degradation. Autophagy and senescence present similar properties where they could exert both cytotoxic or cytoprotective effects, and their interrelationship is complex. Autophagy has been reported to both induce and prevent cell senescence during different processes from oncogene-induced senescence to aging-related muscle cell senescence, yet it could also be the result of the senescence process itself, and many details are yet to be clarified.

Oxidative stress plays a pivotal role in senescence and age-related diseases. Oxidative stress refers to a condition that the amount of reactive oxygen species (ROS) overwhelm the scavenging activity of endogenous antioxidant substances, which results in a range of pathophysiological changes. Mitochondrial ROS (mROS) has been confirmed to be a crucial upstream modulator of autophagy and there are mounting pieces of evidence suggesting the significance of mROS-autophagy crosstalk in cellular homeostasis and survival, and in multiple aging-related pathologies such as metabolic, neurodegenerative, cardiovascular, immune diseases and cancers.

This Special Issue aims to collect original research and review articles regarding the interactions between autophagy and oxidative stress in senescence. Researchers and clinicians are invited to submit basic, translational, or clinical research articles.

Potential topics include but are not limited to the following:

• The understanding of autophagy and oxidative stress in senescence and senescence-related diseases
• The action modes of different phytochemicals in the pathological processes involving autophagy or oxidative stress, including related molecular targets and pathways, metabolisms and pharmacodynamics, and evaluations with bioinformatics
• The progress in the phytochemical selection methods, chemical production, and purification techniques, drug delivery vectors development, pre-clinical and clinical assessments of tolerance, toxicity and therapeutic efficacy, infection control, and malignancy survival benefits
• Pharmacology, pharmacodynamics, pharmacokinetics, and toxicology of autophagy or oxidative stress-targeted compounds in age-related diseases
• Novel delivery systems for chemicals targeting autophagy and oxidative stress
• Potential biomarkers and drug targets in age-related diseases