Connexins (Cx) are members of a protein family that forms intercellular channels localised in gap junction (GJ) plaques and single transmembrane channels called hemichannels. They participate in intercellular communication or communication between the intracellular and extracellular environments. Connexins affect cell homeostasis, growth and differentiation by enabling the exchange of metabolites or by interfering with various signalling pathways. Alterations in the functionality and the expression of connexins have been linked to the occurrence of many diseases. Connexins have been already linked to cancers, cardiac and brain disorders, chronic lung and kidney conditions and wound healing processes. Connexins have been shown either to suppress cancer tumour growth or to increase tumorigenicity by promoting cancer cell growth, migration and invasiveness. A better understanding of the complexity of cancer biology related to connexins and intercellular communication could result in the design of novel therapeutic strategies. The modulation of connexin expression may be an effective therapeutic approach in some types of cancers. Therefore, one important challenge is the search for mechanisms and new drugs, selectively modulating the expression of various connexin isoforms. We performed a systematic literature search up to February 2020 in the electronic databases PubMed and EMBASE. Our search terms were as follows: connexins, hemichannels, cancer and cancer treatment. This review aims to provide information about the role of connexins and gap junctions in cancer, as well as to discuss possible therapeutic options that are currently being studied.

Type 2 diabetes is a disease that causes numerous complications disrupting the functioning of the entire body. Therefore, new treatments for the disease are being sought. Studies in recent years have shown that forkhead box O (FOXO) proteins may be a promising target for diabetes therapy. FOXO proteins are transcription factors involved in numerous physiological processes and in various pathological conditions, including cardiovascular diseases and diabetes. Their roles include regulating the cell cycle, DNA repair, influencing apoptosis, glucose metabolism, autophagy processes and ageing. FOXO1 is an important regulator of pancreatic beta-cell function affecting pancreatic beta cells under conditions of insulin resistance. FOXO1 also protects beta cells from damage resulting from oxidative stress associated with glucose and lipid overload. FOXO has been shown to affect a number of processes involved in the development of diabetes and its complications. FOXO regulates pancreatic β-cell function during metabolic stress and also plays an important role in regulating wound healing. Therefore, the pharmacological regulation of FOXO proteins is a promising approach to developing treatments for many diseases, including diabetes mellitus. In this review, we describe the role of FOXO proteins in the pathogenesis of diabetes and the role of the modulation of FOXO function in the therapy of this disease.

Endocan, previously referred to as an endothelial-cell-specific molecule-1 (ESM-1) is a member of a proteoglycan family that is secreted by vascular endothelial cells of different organs, mainly lungs and kidneys. It is assumed to participate in endothelial activation and the triggering of inflammatory reactions, especially in microvasculatures. Thanks to its solubility in human fluids, i.e., urine and blood plasma, its stability and its low concentrations in physiological conditions, endocan has been proposed as an easily available, non-invasive biomarker for identifying and predicting the course of many diseases. Recently, endocan has been studied in relation to kidney diseases. In general, endocan levels have been linked to worse clinical outcomes of renal dysfunction; however, results are conflicting and require further evaluation. In this review, authors summarize available knowledge regarding the role of endocan in pathogenesis and progression of selected kidney diseases.

Glomerulonephritis (GN) represents a collection of kidney diseases characterized by inflammation within the renal glomeruli and small blood vessels. The lesions that occur in other nephron structures mainly result from the harmful effects of proteinuria. In recent years, an emphasis has been placed on gaining a better insight into the pathogenesis and pathophysiology of GN in order to facilitate diagnoses and provide efficient and targeted treatments of the disease. Owing to the advanced molecular and genetic diagnostic techniques available today, researchers have been able to elucidate that most cases of GN are determined by genetic risk factors and are associated with the abnormal functioning of the immune system (the immunologically mediated forms of GN). MicroRNAs (miRNAs) are a group of single-stranded, non-coding molecules, approximately 20 nucleotides in length, that act as regulatory factors in the post-transcriptional processes capable of regulating the expression of multiple genes. In this paper we present the available research aiming to determine effects of miRNAs on the development and progression of GN and discuss the potential role of miRNAs as new diagnostic markers and therapeutic targets.

The armed aggression of the Russian Federation against Ukraine which started on 24 February 2022 resulted in a massive influx of war refugees from Ukraine. Ukrainian citizens crossed the international borders to flee from the war and apply for an asylum either in Poland or in other EU countries. As many as 115 000 Ukrainians crossed the Polish border in the first 3 days of the Russian invasion. The number grew to 2.3 million over the next 5 weeks. Until July 2023, a total of 13.8 million war refugees crossed the Ukrainian–Polish border on foot, by car or by train. The refugees were predominantly women and children (only ~3% of the war refugees in the given period were men). Until July 2023, 12 million Ukrainians returned from Poland to Ukraine. ¹ At mid-2023 there are ˃3 million Ukrainian citizens living in Poland, including at least 1.3 million economic migrants who had arrived before Russian invasion and 1.8 million war refugees who crossed the Polish border after February 2022. The population in Poland, including 37.5 million Polish nationals, has exceeded 40 million people for the first time in history. ¹ According to the United Nations Refugee Agency, the estimated number of Ukrainian war refugees in the world is 6.3 million as of June 2023, which is the largest migration flow since World War 2 (by comparison, 1.83 million refugees arrived in Europe, mainly from Africa and Asia, during the European migrant crisis in 2015). ²

Insulin resistance is a frequent abnormality in chronic kidney disease (CKD) appearing in early stages. Factors known to promote insulin resistance in CKD patients include disorders of ion and acid–base equilibrium and circulating uremia toxins. Recent research has focused on the central nervous system as the source of the brain-derived neurotrophic factor (BDNF). The aim of our work was to study plasma BDNF concentrations in stage 3 and 4 CKD patients in relationship with insulin resistance and distribution of adipose tissue. Plasma BDNF concentrations were measured in a study group of 31 patients, including a subgroup of 20 non-diabetic subjects. Additionally dual-energy X-ray absorptiometry (DXA) was performed. Homeostatic model assessment of insulin resistance (HOMA-IR) and homeostatic model assessment of B-cell function (HOMA-beta) indices were calculated. Two separate analyses were performed. In the first analysis performed in all 31 CKD patients, there were no correlations between BDNF and: body mass index (BMI), android, gynoid fat distribution, HOMA-IR and HOMA-beta. In the second analysis performed in 20 CKD patients without diabetes, BDNF was negatively related to gynoid fat (Rs = −0.47, P = 0.034) and women revealed significantly lower levels of BDNF than men (P = 0.046). Normotensive patients disclosed significantly higher BDNF levels than hypertensive patients in the whole CKD group (P = 0.039) and in the non-diabetic subgroup (P = 0.028). No correlations between BDNF and eGFR were found. Female sex and arterial hypertension are associated with lower BDNF plasma concentration in CKD patients.