The number of people aged 60 years is expected to increase to 1.4 billion by 2030 and 2.1 billion by 2050. This increase is occurring at an unprecedented pace and will accelerate in coming decades, particularly in developing countries. With the chronological aging, the incidence of several diseases will increase. Indeed, aging is the leading risk factor for impaired mobility, fracture, and multiple non-communicable deadly diseases including cancer, diabetes, cardiovascular diseases and neurodegenerative diseases. Chronological aging correlates with biological aging of organs. The latter results from the cell senescence within tissue, a process that is characterized by a profound rearrangement and reprogramming in cell structure and physiology, leading to the stop of cell growth and eventually death. Signaling pathways and epigenetic mechanisms are the leading mechanisms that orchestrate cell senescence.
In diseases, several pathological stressors, including oxidative stress, mitochondrial dysfunction, and inflammation, could trigger cell senescence. In addition, senescence-associated proteins secreted by senescent cells induce local inflammation and amplify senescence in neighbor cells. Tackling the mechanisms leading to senescence and/or killing specifically senescent cells have recently emerged as new therapeutic strategies for treating non-communicable diseases.
This Article Collection aims at gathering primary research articles, data notes and reviews dealing with the role of molecular mechanisms that drives or tackle cell senescence in non-communicable diseases including (but not limited) cardiovascular, diabetes, cancer, hypertension and neurodegenerative diseases. We strongly encourage submission of in vitro, preclinical and clinical research with multidisciplinary, interdisciplinary and translational approaches.
Potential topics include, but are not limited to
- Epigenetics
- Mitochondria
- Inflammation
- Omics (genomics, metabolomics, transcriptomics, proteomics, kinomics, secretomics)
- Signaling pathways
- Pharmacology
- Drugs
- In silico studies with biological validation
Dr. Stéphane Dalle (SD) is Research Director at the National Institute of Health and Medical Research (INSERM, France). He has a multidisciplinary background including a PhD in Biochemistry & Molecular Biology (Montpellier University, France) and a postdoctoral research degree in Endocrinology & Metabolic Diseases (University of California of San Diego, USA). SD is Director of the laboratory “Innovative Therapeutics for Diabetes” at the Institute of Functional Genomic in Montpellier. He received several awards, INSERM-Avenir, best promising researcher from the Occitanie region. SD has been member of several advisory boards of diabetes associations, industrial companies, and is Section Editor for the Translational Physiology section of All Life.
Dr. Mourad Ferdaoussi (MF) is an Assistant Professor at the University of Alberta (Canada) interested in understanding the molecular and cellular mechanisms involved in the etiology of pancreatic ß cell failure and death in type 2 Diabetes. Dr. Ferdaoussi received his Ph.D. from the University of Lausanne (Switzerland) and did his postdoctoral training at the Montreal Diabetes Research Center (Canada) and the University of Alberta. Dr. Ferdaoussi is a member of the Alberta Diabetes Institute and the Canadian Islet Research and Training Network. Dr. Ferdaoussi received several awards, including the Med Star Postdoctoral and Clinical Fellows from the University of Alberta and Gabriel Baud from the University of Lausanne.
Prof. Amar Abderrahmani (AA) is Full Professor of Cell and Molecular Biology at the Faculty of Medicine at Lille University. He has a multidisciplinary background including a PhD and pharmacy graduation in Molecular genetics and pharmaceutical chemistry. AA has been honored by several Swiss awards and in 2011, of National Chair of Excellence in beta-cell biology, bioscience and diabetes. AA has been member of several scientific committees of Diabetes Association and is currently Editor-in-Chief of All Life.
Disclosure statement: SD, MF, and AA declare no conflict of interest regarding this topic.
