Inflammatory bowel disease is a chronic condition characterized by recurrent intestinal inflammation. Its etiopathogenesis is driven by a series of events that disrupt the mucosal barrier, alter the healthy balance of intestinal microbiota, and abnormally stimulate intestinal immune responses. Therefore, numerous studies suggest the use of short-chain fatty acids and their immunomodulatory effects as a therapeutic approach in this disease. The objective of this systematic review was to synthesize previous evidence on the relevance and therapeutic use of short-chain fatty acids, particularly butyrate, in the immune regulation of inflammatory bowel disease. This systematic review of articles linking inflammatory bowel disease with short-chain fatty acids was conducted according to the PRISMA-2020 guidelines. The Medline and the Web of Science databases were searched in August 2024. The risk of bias was assessed using the Joanna Briggs Institute checklists. A total of 1460 articles were reviewed, of which, 29 met the inclusion criteria. Short-chain fatty acids, particularly butyrate, play a critical role in the regulation of intestinal inflammation and can be used as a strategy to increase the levels of short-chain fatty acid-producing bacteria for use in therapeutic approaches.

Selective targeting of collagen IV in the cancer cell microenvironment reduces tumor burden Selective targeting of collagen IV in the cancer cell microenvironment reduces tumor burden

Goodpasture-antigen binding protein (GPBP) is a nonconventional Ser/Thr kinase for basement membrane type IV collagen. Various studies have questioned these findings and proposed that GPBP serves as transporter of ceramide between the endoplasmic reticulum and the Golgi apparatus. Here we show that cells expressed at least two GPBP isoforms resulting from canonical (77-kDa) and noncanonical (91-kDa) mRNA translation initiation. The 77-kDa polypeptide interacted with type IV collagen and localized as a soluble form in the extracellular compartment. The 91-kDa polypeptide and its derived 120-kDa polypeptide associated with cellular membranes and regulated the extracellular levels of the 77-kDa polypeptide. A short motif containing two phenylalanines in an acidic tract and the 26-residue Ser-rich region were required for efficient 77-kDa polypeptide secretion. Removal of the 26-residue Ser-rich region by alternative exon splicing rendered the protein cytosolic and sensitive to the reduction of sphingomyelin cellular levels. These and previous data implicate GPBPs in a multicompartmental program for protein secretion (i.e. type IV collagen) that includes: 1) phosphorylation and regulation of protein molecular/supramolecular organization and 2) interorganelle ceramide trafficking and regulation of protein cargo transport to the plasma membrane.

Background/Objectives: Endocrine disruptors are substances capable of altering the functions of the endocrine system. There is evidence that some pesticides can be endocrine disruptors and, among some of their effects, we find alterations in pubertal development and in the function of the thyroid gland, which could be related to a greater tendency of obesity. The aim was to evaluate the evidence from clinical and preclinical studies on the association between pesticides used in agriculture and found in plant-based foods with overweight/obesity. Methods: This is a systematic review of articles on the impact of the use of endocrine disrupting pesticides on obesity, conducted according to the PRISMA-2020 guidelines. Results: There was evidence that some pesticides, such as chlorpyrifos, pyrethroids, and neonicotinoids, may promote obesity and other anthropometric changes by altering lipid and glucose metabolism, modifying genes, or altering hormone levels such as leptin. Other studies suggest that perinatal exposure to chlorpyrifos or pesticides such as vinclozolin may alter lipid metabolism and promote weight gain in adulthood, whereas other pesticides such as boscalib, captan, thiacloprid, and ziram were not associated with changes in weight. Exposure to pesticides such as vinclozolin may be associated with a higher prevalence of overweight/obesity in later generations. Conclusions: The few studies that do not show these associations have methodological limitations in data collection with confounding variables. Further studies are needed to provide more and higher quality evidence to determine the true effect of these substances on obesity.

Collagen, a versatile family of proteins with 28 members and 44 genes, is pivotal in maintaining tissue integrity and function. It plays a crucial role in physiological processes like wound healing, hemostasis, and pathological conditions such as fibrosis and cancer. Collagen is a target in these processes. Direct methods for collagen modulation include enzymatic breakdown and molecular binding approaches. For instance, Clostridium histolyticum collagenase is effective in treating localized fibrosis. Polypeptides like collagen-binding domains offer promising avenues for tumor-specific immunotherapy and drug delivery. Indirect targeting of collagen involves regulating cellular processes essential for its synthesis and maturation, such as translation regulation and microRNA activity. Enzymes involved in collagen modification, such as prolyl-hydroxylases or lysyl-oxidases, are also indirect therapeutic targets. From another perspective, collagen is also a natural source of drugs. Enzymatic degradation of collagen generates bioactive fragments known as matrikines and matricryptins, which exhibit diverse pharmacological activities. Overall, collagen-derived peptides present significant therapeutic potential beyond tissue repair, offering various strategies for treating fibrosis, cancer, and genetic disorders. Continued research into specific collagen targeting and the application of collagen and its derivatives may lead to the development of novel treatments for a range of pathological conditions.

Liver cancer, particularly hepatocellular carcinoma, is a global concern. This study focuses on the evaluation of Atezolizumab and Bevacizumab combination therapy as a promising alternative in the treatment of advanced hepatocellular carcinoma. The objectives of this systematic review include evaluating the efficacy of Atezolizumab and Bevacizumab combination therapy compared to conventional therapies with Sorafenib and other conventional therapies, analyzing the associated adverse effects, and exploring prognostic factors in the setting of advanced hepatocellular carcinoma. A systematic literature review was carried out using the PubMed and Web of Science databases. Fifteen related articles were included and evaluated according to their level of evidence and recommendation. Results: The combination therapy of Atezolizumab and Bevacizumab, along with Sorafenib, showed positive results in the treatment of patients with advanced hepatocellular carcinoma. Significant adverse effects were identified, such as gastrointestinal bleeding, arterial hypertension, and proteinuria, which require careful attention. In addition, prognostic factors, such as transforming growth factor beta (TGF-β), alpha-fetoprotein (AFP), and vascular invasion, were highlighted as key indicators of hepatocellular carcinoma progression. Conclusions: The combination of Atezolizumab and Bevacizumab is shown to be effective in the treatment of advanced hepatocellular carcinoma, although it is essential to take into consideration the associated adverse effects. The prognostic factors identified may provide valuable information for the clinical management of this disease. This study provides a comprehensive overview of a promising emerging therapy for liver cancer.