OBM Geriatrics

(ISSN 2638-1311)

OBM Geriatrics is an Open Access journal published quarterly online by LIDSEN Publishing Inc. The journal takes the premise that innovative approaches – including gene therapy, cell therapy, and epigenetic modulation – will result in clinical interventions that alter the fundamental pathology and the clinical course of age-related human diseases. We will give strong preference to papers that emphasize an alteration (or a potential alteration) in the fundamental disease course of Alzheimer’s disease, vascular aging diseases, osteoarthritis, osteoporosis, skin aging, immune senescence, and other age-related diseases.

Geriatric medicine is now entering a unique point in history, where the focus will no longer be on palliative, ameliorative, or social aspects of care for age-related disease, but will be capable of stopping, preventing, and reversing major disease constellations that have heretofore been entirely resistant to interventions based on “small molecular” pharmacological approaches. With the changing emphasis from genetic to epigenetic understandings of pathology (including telomere biology), with the use of gene delivery systems (including viral delivery systems), and with the use of cell-based therapies (including stem cell therapies), a fatalistic view of age-related disease is no longer a reasonable clinical default nor an appropriate clinical research paradigm.

Precedence will be given to papers describing fundamental interventions, including interventions that affect cell senescence, patterns of gene expression, telomere biology, stem cell biology, and other innovative, 21st century interventions, especially if the focus is on clinical applications, ongoing clinical trials, or animal trials preparatory to phase 1 human clinical trials.

Papers must be clear and concise, but detailed data is strongly encouraged. The journal publishes research articles, reviews, communications and technical notes. There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.

Archiving: full-text archived in CLOCKSS.

Rapid publication: manuscripts are undertaken in 12 days from acceptance to publication (median values for papers published in this journal in 2021, 1-2 days of FREE language polishing time is also included in this period). 

Current Issue: 2023  Archive: 2022 2021 2020 2019 2018 2017

Special Issue

Recent Breakthroughs in Ageing Research: Senolytic Drugs to Fight Senescent Cells as an Anti-ageing Strategy

Submission Deadline: December 15, 2023 (Open) Submit Now

Guest Editor

Calogero Caruso, MD, Professor

Laboratory of Immunopathology and Immunosenescence, Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy

Website | E-Mail

Research Interests: Aging; Diseases related to age and longevity, immunosenescence and immunopathology

About This Topic

This special issue of OBM Geriatrics will explore one of the latest scientific researches in the field of ageing, namely, the role of senolytic treatment in fighting the ageing process.

Cellular senescence, a process characterized by irreversible cell cycle arrest with peculiar secretory characteristics, macromolecular damage, and impaired metabolism, is implicated in ageing and is associated with a broad spectrum of age-related diseases. Cellular senescence can be triggered by several stress signals to the cell, including DNA damage, telomere shortening, oncogene activation or loss of tumor suppressive functions, mitochondrial dysfunction, nutrient deprivation, hypoxia, and epigenetic changes. The impaired mitochondrial function is responsible for the elevated production of reactive oxygen species, which in turn can drive the activation of NF-kB, thus inducing the senescence-associated secretory phenotype (SASP). SASP is a hallmark of senescence and mediates many of its pathophysiological effects. Senescent cells secrete bioactive molecules, particularly pro-inflammatory cytokines and chemokines that contribute to inflamm-ageing associated with age-related diseases, frailty, and mortality in older people. Senescent cells accumulate with age in multiple tissues and can cause functional decline of the organism. Senescence also affects the immune system. A mouse model with selective deletion of a DNA damage repair protein in hematopoietic cells has been created to induce senescence only in the immune system. Surprisingly, the non-lymphoid organs of these mice also showed increased markers of senescence, suggesting that a senescent immune system has a causal role in driving organismal ageing.

So, it is not surprising that increasing efforts have been devoted identifying drugs that specifically target senescent cells by inducing apoptosis, drugs that have been named senolytics. Natural or synthetic compounds with senolytic activity, i.e., the ability to selectively remove senescent cells by inducing apoptosis, and immunotherapies using immune cell-mediated clearance of senescent cells are currently the most promising strategies to fight ageing and age-related diseases. Indeed, pharmacological strategies aimed to reverse cellular senescence and SASP are hot topics in the framework of anti-ageing strategy. Several drugs that target gene products that protect senescent cells from apoptosis have been tested for their ability to eliminate senescent cells in vitro. Moreover, it has been reported that chimeric antigen receptor (CAR) T cells can be redirected to target senescent cells in animal models. CAR T cells that specifically target senescent cells could be a further senolytic treatment strategy for senescence-associated diseases. This special issue will feature the most recent research on the efficacy of many senolytic treatments, particularly drugs of botanical origin, in eliminating senescent cells. This special issue will welcome both original papers and reviews on whether and which treatments can effectively delay, prevent and/or reverse aging. may involve in vitro and in vivo studies in different cells and organisms.


Cellular senescence; SASP; Senolytic drugs