Heat shock proteins (Hsps) are involved in one of the adaptive mechanisms protecting cells against environmental and metabolic stress. Moreover, the large role of these proteins in the carcinogenesis process, as well as in chemoresistance, was noticed. This review aims to draw attention to the possibilities of using Hsps in developing new cancer therapy methods, as well as to indicate directions for future research on this topic. In order to discuss this matter, a thorough review of the latest scientific literature was carried out, taking into account the importance of selected proteins from the Hsp family, including Hsp27, Hsp40, Hsp60, Hsp70, Hsp90 and Hsp110. One of the more characteristic features of all Hsps is that they play a multifaceted role in cancer progression, which makes them an obvious target for modern anticancer therapy. Some researchers emphasize the importance of directly inhibiting the action of these proteins. In turn, others point to their possible use in the design of cancer vaccines, which would work by inducing an immune response in various types of cancer. Due to these possibilities, it is believed that the use of Hsps may contribute to the progress of oncoimmunology, and thus help in the development of modern anticancer therapies, which would be characterized by higher effectiveness and lower toxicity to the patients.

Glutathione S-transferases are a family of enzymes, whose main role is to detoxify cells from many exogenous factors, such as xenobiotics or carcinogens. It has also been proven that changes in the genes encoding these enzymes may affect the incidence of selected cancers and cardiovascular diseases. The aim of this study was to review the most important reports related to the role of glutathione S-transferases in the pathophysiology of two of the most common diseases in modern society – cancers and cardiovascular diseases. It was shown that polymorphisms in the genes encoding glutathione S-transferases are associated with the development of these diseases. However, depending on the ethnic group, the researchers obtained divergent results related to this field. In the case of the GSTP1 A/G gene polymorphism was shown an increased incidence of breast cancer in Asian women, while this relationship in European and African women was not found. Similarly. In the case of cardiovascular diseases, the differences in the influence of GSTM1, GSTT1, GSTP1 and GSTA1 polymorphisms on their development or lack of it depending on the continent were shown. These examples show that the development of the above-mentioned diseases is not only influenced by genetic changes, but their pathophysiology is more complex. The mere presence of a specific genotype within a studied polymorphism may not predispose to cancer, but in combination with environmental factors, which often depend on the place of residence, it may elevate the chance of developing the selected disease.

Background: Angiotensin-converting enzyme (ACE) is responsible for the production of angiotensin II, and increased production of angiotensin II is observed in diabetes. What is more, ACE polymorphisms may play a role in the development of diabetic nephropathy. The aim of this study was to assess the role of selected ACE polymorphisms (rs4343 and rs4646994) in the risk of development of diabetic nephropathy and in the likelihood of renal replacement therapy. Methods: ACE polymorphisms were analyzed in a group of 225 patients who were divided into three subgroups. The rs4343 polymorphism was determined using the PCR-RFLP, and the rs4646994 polymorphism was determined using the PCR. Molecular docking between domains of ACE and its ligands was performed by using AutoDock Vina. Results: The G/G genotype of rs4343 polymorphism is associated with increased odds of developing diabetic nephropathy. The G allele is also associated with a higher risk of this disease. Similar results were obtained in patients who had already had a kidney transplant as a result of diabetic nephropathy. Conclusions: The presence of G/G and G/A genotypes, and the G allele increases the likelihood of developing diabetic nephropathy. This may also be a risk factor for renal replacement therapy.

Obesity and diabetes are a problem of modern medicine. Although the environmental factors contributing to the development of these diseases are widely known, research into genetic factors is still ongoing. At the same time, the role of inflammation in the pathophysiology of obesity and diabetes is increasingly emphasized. Therefore, the purpose of this study was to investigate the influence of two selected polymorphisms (rs1800795 and rs3842729) on the development of obesity and type 2 diabetes. In this study, 118 participants were examined, including a control group (nonobese and nondiabetic group), an obese group, and a diabetic group. Genotype analysis was performed using the PCR‐RFLP method. It has been shown that in patients with the G/G genotype within the rs1800795 polymorphism (IL6) , the chance of developing type 2 diabetes is several times lower compared to patients with the G/C and C/C genotypes. However, the rs3842729 polymorphism (INS) does not directly affect the risk of obesity or type 2 diabetes (T2D), although elevated insulin concentrations have been observed in obese and diabetic patients. These results confirm the impact of the rs1800795 polymorphism on the development of diabetes; however, this relationship is more complex and requires further research on other factors.

Background: Nitric oxide synthase (NOS) is an enzyme that catalyzes the formation of nitric oxide (NO), the altered production of which is characteristic of diabetic nephropathy. NOS exists in three isoforms: NOS1, NOS2, and NOS3. Moreover, there are reports about the potential role of NOS3 polymorphisms in the development of diabetes complications. The aim of this study was to assess the role of selected NOS polymorphisms—rs3782218 (NOS1), rs1137933 (NOS2), rs1799983, rs2070744, and rs61722009 (NOS3)—in the risk of developing diabetic nephropathy and in the likelihood of renal replacement therapy. Methods: The studied polymorphisms were analyzed in a group of 232 patients divided into three groups. Four polymorphisms (rs3782218, rs1137933, rs1799983, rs2070744) were genotyped using the PCR-RFLP, while the rs61722009 polymorphism was genotyped using the PCR. Results: The C/C genotype and the C allele of the rs3782218 polymorphism (NOS1) were associated with an increased risk of developing diabetic nephropathy and an increased likelihood of renal replacement therapy. In turn, the G allele of the rs1137933 polymorphism (NOS2) reduces the likelihood of renal replacement therapy. Conclusions: The specific genotypes or alleles of the rs3782218 (NOS1) and rs1137933 (NOS2) polymorphisms seem to be potential risk factors for diabetic nephropathy and renal replacement therapy.

Due to their prevalence, diabetes and its complications continue to pose a significant challenge in modern medicine. It is particularly important to identify and develop new biomarkers that would enable faster and more effective detection of specific diseases, including the most common complication of diabetes—diabetic kidney disease (DKD). This review presents the current knowledge on two proteins—fetuin-A and heme oxygenase 1 (HO-1)—whose biological functions and involvement in the pathophysiology of the discussed disease make them potentially useful biomarkers. Moreover, there are studies indicating an association of polymorphisms in the genes encoding fetuin-A and HO-1 with the risk of developing diabetes or DKD. Based on the available literature, both proteins appear promising for use in the diagnosis of diabetes and its complications or assessing the risk of these diseases. However, this requires confirmation in large-scale studies and the development and standardization of detection methods.