The technostress model has introduced different factors to consider when assessing how information and communication technologies impact individuals in different work settings. This systematic review gathers evidence regarding associations between occupational exposure to technostress and health or work outcomes. In addition, we highlight typical methodological constraints of the technostress model. We conducted electronic literature searches in June 2020 (PubMed, PubMed Central, Web of Science, Scopus, PsycInfo, PsycArticles) and independently screened 321 articles. We report on 21 articles meeting eligibility criteria (working population, technostress exposure, health or work outcome, quantitative design). The most frequently examined techno-stressors, i.e., factors of technostress, were techno-overload and techno-invasion. Techno-stressors were consistently associated with adverse health and work outcomes, apart from a positive impact on work engagement. However, studies may be subject to considerable conceptual overlap between exposure and outcome measures. Future technostress research would benefit from reducing heterogeneity in technostress measures, assessing their external validity and focussing on specific techno-stressors.

In addition to its catastrophic health effects, the COVID-19 pandemic also acts as a catalyst for new forms of work. Working from home (WFH) has become commonplace for many people worldwide. But under what circumstances is WFH beneficial and when does it increase harms to health? The aim of this study was to investigate the influence of specific characteristics of WFH for health (work ability, stress-related physical and psychological symptoms) and job satisfaction among German employees. The study is based on data from a Germany-wide panel survey with employees from different industries (n = 519). Using multiple regressions, it was found that the functionality of the technical equipment at home has positive effects on the health of employees (i.e., ability to work, stress-related symptoms) and job satisfaction. The percentual weekly amount of WFH influences stress-related symptoms, i.e., a higher amount of weekly working time WFH, was associated with more stress-related symptoms. Furthermore, it negatively influences job satisfaction. The feeling of increased autonomy leads to positive effects on employees’ job satisfaction. The results provide starting points for interventions and indicate the need for legal regulations for WFH. Further theoretical and practical implications are discussed.

Cardiovascular diseases (CVD) increasingly burden societies with vast financial and health care problems. Therefore, the importance of improving preventive and therapeutic measures against cardiovascular diseases is continually growing. To accomplish such improvements, research must focus particularly on understanding the underlying mechanisms of such diseases, as in the field of epigenetics, and pay more attention to strengthening primary prevention. To date, preliminary research has found a connection between DNA methylation, histone modifications, RNA-based mechanisms and the development of CVD like atherosclerosis, cardiac hypertrophy, myocardial infarction, and heart failure. Several therapeutic agents based on the findings of such research projects are currently being tested for use in clinical practice. Although these tests have produced promising data so far, no epigenetically active agents or drugs targeting histone acetylation and/or methylation have actually entered clinical trials for CVDs, nor have they been approved by the FDA. To ensure the most effective prevention and treatment possible, further studies are required to understand the complex relationship between epigenetic regulation and the development of CVD. Similarly, several classes of RNA therapeutics are currently under development. The use of miRNAs and their targets as diagnostic or prognostic markers for CVDs is promising, but has not yet been realized. Further studies are necessary to improve our understanding of the involvement of lncRNA in regulating gene expression changes underlying heart failure. Through the data obtained from such studies, specific therapeutic strategies to avoid heart failure based on interference with incRNA pathways could be developed. Together, research and testing findings raise hope for enhancing the therapeutic armamentarium. This review presents the currently available data concerning epigenetic mechanisms and compounds involved in cardiovascular diseases, as well as preventive and therapeutic approaches against them.

Consolidated knowledge is accumulating as to the role of epigenetic regulatory mechanisms in the physiology of vascular development and vascular tone as well as in the pathogenesis of cardiovascular disease. The modulation of gene expression through modification of the epigenome by structural changes of the chromatin architecture without alterations of the associated genomic DNA sequence is part of the cellular response to environmental changes. Such environmental conditions, which are finally being translated into adaptations of the cardiovascular system, also comprise pathological conditions such as atherosclerosis or myocardial infarction. This review summarizes recent findings on the epigenetics of vascular regulation and disease and presents nutritional and pharmacological approaches as novel epigenetic strategies in the prevention and treatment of cardiovascular disease.

Sirtuin 5 (SIRT5) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase and belongs to the Silent information regulator 2 (Sir2) family of sirtuin histone deacetylases (HDACs), which play a central role in epigenetic gene silencing, DNA repair and recombination, cell-cycle, microtubule organization, and in the regulation of aging. We have isolated and characterized the human SIRT5 genomic sequence, which spans a region of 28,182 bp and which has one single genomic locus. Human SIRT5 consists of eight exons and is found in two isoforms, which encode a 310 aa and a 299 aa protein, respectively. Human SIRT5 is most predominantly expressed in heart muscle cells and in lymphoblasts. Fluorescence in situ hybridization analysis localized the human SIRT5 gene to chromosome 6p23.