An increasing number of scientific reports on the mechanisms of cell death is seeing light. Especially publications on the different processes of programmed cell death are getting major attention. For example, insight has been provided in the interaction between linear ubiquitination, regulators of cell death and type I interferon responses by OTULIN, thereby limiting cell death and inflammation [1]. Another important finding shows insight in the regulation of RNA decay in cells. This appears to be regulated by release of the mitochondrial intermembrane space 3′–5′-exoribonuclease PNPT1 during apoptosis [2]. In a large cohort of early stage invasive breast cancer patients it was found that caspase-3 expression was associated to adverse cancer-specific survival [3]. The impact of these observations underline that it is of extreme importance to understand the mechanisms of cell death, in order to understand e.g. the mechanisms of disease. These observations also clearly demonstrate that cell death lives.

From the editors’ desks

To better being able to serve the scientific community, the publisher and editors have embarked on a track to rejuvenate Apoptosis and implement a few changes to the appearance of the journal [4]. First of all, we decided to use of an award winning image on cell death for the cover of the journal. Last year’s cover was an image provided by Dr. Ivan Poon (Victoria, Australia) showing the beaded apoptopodia of an ultraviolet light treated monocytic cell [5, 6]. The 2019 volume will be covered by a dramatic electron microscopy image of an apoptotic cell, contributed by Dr. Walter Malorni and Dr. Antonella Tinari. This picture represents an MDCK dog kidney cell infected with influenza virus strain WSN and treated with the caspase inhibitor z-Vad [7, 8]. Infection of a cell by influenza A virus leads to apoptotic cell death. However, elevated lysosomal activity and an abundance of autophagosomes can be observed when apoptosis is inhibited. Hence, the balance between apoptotic mechanisms and autophagic cytoprotection pathway is essential for successful viral spreading or its abortive replication. On the cell side, apoptotic cell death or autophagic cell survival can in turn be pivotal in the pathogenetic mechanisms of infection. General processes occurring during apoptosis, such as cell surface blebbing, viral budding from the cell membrane and chromatin marginalization are clearly visible in the new cover image [9, 10].

Another change to the journal is that we reduced the number of accepted manuscripts and joined two issues together in one printed release. We hope that these measures will lead to increased recognition and impact of Apoptosis. Finally, a small market survey in the field indicated that the journal name Apoptosis may limit the scope of the journal, despite the provided subtitle An International Journal on Programmed Cell Death. The result of this survey started a discussion on a possible name change of the journal in the future.

The editors’ choice

The general interest in research on cell death is also visible in the submissions to Apoptosis. The majority of submitted papers represent the fields of cardiovascular disease and cancer, where it is clear that cell death processes play key roles in the pathology of the disease.

A number of recently published papers should be highlighted. It was found that the mechanism by which diallyl trisulfide protects against apoptosis during myocardial ischemia–reperfusion injury in diabetic disease, involves activation of silent information regulator-1 (SIRT1) [11]. Another paper related to cardiovascular disease reports on the role of stromal cell-derived factor-1 (SDF-1) in stimulating TNF-mediated apoptosis in cardiac myocytes. Isolated rat cardiac myocytes treated with SDF-1 undergo apoptosis, suggesting the importance of SDF-1 in regulating the cardiomyocyte response to stress conditions [12]. In the field of cancer several submissions to the journal stood out. One paper reported on the pentahydroxyflavone Quercetin to induce protective autophagy and apoptosis via the STAT3/Bcl-2 pathway in ovarian cancer cells. The authors suggested that this finding provides a new angle to circumvent drug resistance in patients by targeting protective autophagy pathways [13]. Another interesting paper reports on the promotion of cytotoxic autophagy and apoptosis in phenotypically different breast cancer cells by affecting the glycolytic pathway by ursolic acid [14]. In cervical cancer HeLa cells it was shown that piperazine suppresses proliferation and migration, but induced apoptosis. This paper suggested a new compound for the development of an effective antitumor agent [15]. Apoptosis also published a number of excellent reviews as well. Rathore et al. published on the bypassing drug resistance in cancer by targeting inhibitors of apoptosis proteins (IAPs). In this paper mimetics of second mitochondria-derived activator of caspase (SMAC) are highlighted as potential agents to treat cancer [16]. Circumvention of negative regulators of cell death is a major challenge in cancer research, as these molecules can be important in the development of drug induced resistance. A review by Razaghi et al. presents this potential arena for drug discovery and biomarker development [17]. Another paper reviews the strategies of inducing reactive oxygen species in cancer cells, as an approach for anticancer therapy [18]. Outside the field of cancer two excellent reviews were published. One of these was on the role of endoplasmic reticulum (ER) stress in neurodegenerative disease. Unfolded protein response is a cellular response to ER stress. Dysfunction of this process plays an important role in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and Huntington’s disease by the accumulation and aggregation of misfolded proteins. It is suggested that inhibition of specific ER mediators may contribute to the treatment and prevention of neurodegeneration [19]. Last but not least to mention is the paper that reviews the apoptosis-induced lymphopenia in sepsis and severe injuries. These conditions are usually followed by a period of marked immunosuppression. It is suggested that apoptosis targeting strategies can be applied to intervene in patients with such conditions [20]. Apoptosis will continue the effort of publishing high-impact publications.