Lung fibrosis is a consequence of many influences leading to damage to lung tissue and the development of subsequent inflammation. Fibrosis is an overgrowth of connective tissue, which can lead to a violation of the architectonics of the lungs and reduce their functionality up to a fatal outcome. At the same time, the mechanisms underlying fibrogenesis are currently insufficiently studied. In this regard, the task of studying them does not lose its relevance, and its solution requires the development of models of lung fibrosis that can reflect all the key processes of fibrogenesis.

The in vivo model using animals has multiple undeniable advantages, but at the same time it has strict ethical limitations and does not reflect all the mechanisms of lung fibrosis inherent in the human body. At the same time, in vitro research, scientists can afford to use biomaterials not only of animals, but also of humans, and build cellular systems based on them — from 2D to 3D models. Modeling of pulmonary fibrosis is mainly based on the use of the main types of cells involved in the development of pulmonary fibrosis, such as myofibroblasts, fibroblasts, alveolocytes and others. Some models are also based on a specific fibrosis-associated extracellular matrix and further study of the interaction of cells with each other and with the matrix. It should be borne in mind that different models display individual nuances of the native processes of lung fibrogenesis, which requires the research community to use a wide range of models. Taking into account the multifactorial pathogenesis of pulmonary fibrosis, it is important to understand the totality of the processes taking place in order to obtain the completeness of the real picture, close to the picture in vivo, and therefore the multicomponence of models is important. This review focuses on the analysis of various models of lung fibrosis in vitro in two-dimensional and three-dimensional systems, shows approaches to their creation, key differences, main advantages and disadvantages of models, both particular and general.

Regenerative medicine aims at changing modern medicine practice by eliminating core reasons of diseases and disorders. Regenerative medicine includes gene therapy, cell therapy and products of tissue engineering that are destined for augmentation, regeneration or replacement of organs, tissues, genes and metabolic processes in the organism. Biomaterials are amongst key components of regenerative medicine on which successful strategies are based.

The review of biotechnological methods implemented in the USP and DSP stages with the use of B. mori was made. The methods analysed are aimed at improving quality characteristics and obtaining new kinds of biomaterials to meet the needs of regenerative medicine and biomedicine. The diversity of biotechnological solutions that allow to gain a wide spectrum of biomaterials (incl. derivatives of cocoon shell such as fibroin, sericin and their composites; recombinant derivatives; antimicrobial peptides; modified transgenic silk fibres;transgenic fibres that contain growth factors and peptides; etc.) is a unique basis for the bioindustrial platform on the B. mori basis.

The promise of genome editing technologies (GETs) for gene therapy is one of the key drivers for development of this field to treat monogenic hereditary diseases. However, the general consensus of research community and many physicians is that in some cases the balance of risk and benefit of GET-based drugs and CRISPR/Cas9, in particular, has not been fully studied to date. However, on December 03, 2023, the US Food and Drug Administration (FDA) approved marketing of two products for sickle cell disease. One of them (“Casgevy”) is a cellular product consisting of CD34+ autologous hematopoietic stem cells, in which, using the CRISPR/Cas9 system, it was possible to increase the production of fetal hemoglobin, which leads to compensation of patient’s condition. Thus, for the first time in world practice, national regulator has approved not just a genetically modified cell product, but a product obtained using GET. This short message is dedicated to this historical event and its importance, as well as possible consequences.

Angiogenesis plays a crucial role in tissue and organ regeneration by supplying essential nutrients and oxygen through the development of new blood vessels. Mesenchymal stem/stromal cells release extracellular vesicles that actively contribute to angiogenesis by carrying pro-angiogenic growth factors and microRNAs. MicroRNAs, small non-coding RNA molecules, are central players in angiogenesis, affecting endothelial cell proliferation, specialization, migration, apoptosis, and post-transcriptional gene expression.

In the present study, we investigated the impact of extracellular vesicles containing Plaur-miR1- 5p microRNAs on angiogenesis, specifically focusing on its initial stages: vascular cell migration and the formation of capillary-like structures. Recently we discovered Plaur-miR1-5p, which is encoded within the urokinase receptor gene (Plaur). However, the functions of this microRNA remain largely unexplored. Using a vascular ring model embedded in Matrigel, we demonstrate that Plaur-miR1-5p is encapsulated within extracellular vesicles and plays a regulatory role in capillary-like structure formation. Moreover, applying bioinformatic analysis, we have identified potential target genes of Plaur-miR1-5p that participate in the regulation of angiogenesis.

This study advances our comprehension of the fundamental processes governing angiogenesis, particularly the involvement of extracellular vesicles and microRNAs. Moreover, it sheds light on the functional aspects ofthe Plaur gene, contributing to a more profound understanding of its role in regulation of angiogenesis.

Neuroinflammation is considered as one of the mechanisms by which stress can potentially lead to a disturbance of the functions of the central nervous system. The presence of neuroimmune dysfunction after stress, and what genetic factors increase the risk of post-stress neuroinflammation has not been sufficiently investigated. Genetically determined excitability of the nervous system is a promising marker of individual vulnerability to stress, manifested in post-stress disorders associated with the specifics of the formation of neuroinflammation.

The aim of this work was to study post-stress changes in the expression of pro-inflammatory il-6 genes in the blood and hippocampus and anti-inflammatory cytokine bdnf in the blood of rats with genetically determined high and low levels of excitability of the nervous system. Breeding animals were used, males of two strains of rats aged 5 months: with a high threshold (HT) of excitability of the nervous system (low excitable) and a low threshold (LT) of excitability of the nervous system (high excitable) from the biological collection of the Pavlov Institute of Physiology of the Russian Academy of Sciences. The stress model is a long-term emotional and painful stress according to the scheme of K. Hecht. Experimental and control animals were decapitated 24 hours, 7 days and 24 days after the end of stress exposure. Changes in the mRNA level of the il-6 and bdnf genes were evaluated using real-time PCR.

Chronic stress led to a significant increase in the level of il-6 mRNA in the hippocampus only in high excitable animals 24 days after the end of stress. In the blood, the mRNA level of this cytokine increased only in low-excitable rats. The expression of the bdnf gene in blood did not change in response to stress in any of the strains.