Chronic kidney disease (CKD) is characterized by renal parenchymal damage leading to a reduction in the glomerular filtration rate. The inflammatory response plays a pivotal role in the tissue damage contributing to renal failure. Current therapeutic options encompass dietary control, mineral salt regulation, and management of blood pressure, blood glucose, and fatty acid levels. However, they do not effectively halt the progression of renal damage. This review critically examines novel therapeutic avenues aimed at ameliorating inflammation, mitigating extracellular matrix accumulation, and fostering renal tissue regeneration in the context of CKD. Understanding the mechanisms sustaining a proinflammatory and profibrotic state may offer the potential for targeted pharmacological interventions. This, in turn, could pave the way for combination therapies capable of reversing renal damage in CKD. The non-replacement phase of CKD currently faces a dearth of efficacious therapeutic options. Future directions encompass exploring vaptans as diuretics to inhibit water absorption, investigating antifibrotic agents, antioxidants, and exploring regenerative treatment modalities, such as stem cell therapy and novel probiotics. Moreover, this review identifies pharmaceutical agents capable of mitigating renal parenchymal damage attributed to CKD, targeting molecular-level signaling pathways (TGF-β, Smad, and Nrf2) that predominate in the inflammatory processes of renal fibrogenic cells.

Chronic kidney disease (CKD) is a progressive disease with a high mortality rate and a worldwide prevalence of 13.4%, triggered by various diseases with high incidence. The aim of the present study was to investigate the anti‑inflammatory and antifibrotic effect of pioglitazone on kidney in an adenine‑induced Wistar rats and the mechanisms possibly involved. CKD was induced in 40 rats. Rats were divided into two groups, which were split into the following sub‑groups: i) Therapeutic (pioglitazone administered after renal damage) divided into intact (healthy), adenine (CKD) and adenine/pioglitazone (treatment) and ii) prophylactic (adenine and pioglitazone administered at the same time) split into intact (healthy), adenine (CKD), endogenous reversion (recovery without treatment), adenine/pioglitazone (treatment) and pioglitazone sub‑groups. Reverse transcription‑quantitative PCR (collagen I, α‑SMA and TGF‑β), and hematoxylin‑eosin, Masson's trichrome and Sirius red staining were performed to measure histological markers of kidney damage, also the serum markers (urea, creatinine and uric acid) were performed, for analyze the effects of pioglitazone. In the adenine/pioglitazone rats of the therapeutic group, renal function parameters such as eGFR increased and serum creatinine decreased from those of untreated rats (CKD), however the renal index, serum urea, abnormalities in renal morphology, inflammatory cells and relative gene expression of collagen I, α‑SMA and TGF‑β did not change relative to the CKD rats. In adenine/pioglitazone rats, extracellular matrix collagen accumulation was significantly lower than the CKD rats. On the other hand, in adenine/pioglitazone rats of the prophylactic group, the renal index, creatinine, urea, uric acid serum and relative gene expression of collagen I, α‑SMA, and TGF‑β were significantly lower, as well as the presence of 2,8‑dihydroxyadenine crystals, and extracellular matrix collagen compared with CKD rats. In addition, the eGFR in the treatment group was similar to healthy rats, renal morphology was restored, and inflammatory cells were significantly lower. In conclusion, pioglitazone has a nephroprotective effect when administered in the early stages of kidney damage, reducing inflammatory and fibrotic processes and improving glomerular filtration rate. Furthermore, in the late phase of treatment, a tendency to decrease creatinine and increase eGFR was observed.

Non-alcoholic fatty liver disease (NAFLD) is an emerging condition with a worldwide prevalence ranging from 6% to 35% and is very frequent among patients with obesity, diabetes, or metabolic syndrome. One of the main challenges in the treatment of this disease is the identification of a reliable and direct biomarker to diagnose the stage of hepatic steatosis before it progresses to steatohepatitis. This is especially important as many patients remain asymptomatic until cirrhosis develops. The aim of this study was to analyze the expression of the enzyme acetyl-CoA carboxylase 1 (ACC-1) in vitro in a model of lipocytotoxicity using HepG2 cells as well as in vivo in Wistar rats. Our results demonstrate an accumulation of lipid inclusions in hepatocytes observed both in vitro and in experimental models of hepatic steatosis, leading to membrane damage. This allows for the detection of ACC-1 enzyme in the extracellular medium at short induction times, in contrast to the appearance of AST and ALT, which become detectable only once the damage becomes more invasive. ACC-1 could potentially serve as a clinical indicator to detect fatty liver disease before it progresses to steatohepatitis and fibrosis, allowing for timely and non-invasive treatment for patients.

We investigated the influence of gold deposition on the magnetic behavior, biocompatibility, and bioactivity of CoFe₂O₄ (MCF) nanomaterials (NMs) functionalized with sodium citrate (Cit) or glycine (Gly). The resulting multifunctional plasmonic nanostructured materials (MCF-Au-L, where L is Cit, Gly) exhibit superparamagnetic behavior with magnetic saturation of 59 emu/g, 55 emu/g, and 60 emu/g, and blocking temperatures of 259 K, 311 K, and 322 K for pristine MCF, MCF-Au-Gly, and MCF-Au-Cit, respectively. The MCF NMs exhibit a small uniform size (with a mean size of 7.1 nm) and an atomic ratio of Fe:Co (2:1). The gold nanoparticles (AuNPs) show high heterogeneity as determined by high-resolution transmission electron microscopy (HR-TEM) and energy-dispersive X-ray spectroscopy (EDX). The UV-Vis spectroscopy of the composites reveals two localized surface plasmons (LSPs) at 530 nm and 705 nm, while Fourier Transformed-Infrared spectroscopy (FTIR) and thermogravimetric analysis (TGA) confirm the presence of Cit and Gly on their surface. Subsequent biocompatibility tests confirm that MCF-Au-L NMs do not exert hemolytic activity (hemolysis < 5%). In addition, the CCK-8 viability assay tests indicate the higher sensitivity of cancerous cells (A549) to the photoactivity of MCF-Au compared to healthy Detroit 548 (D548) cell lines. We use advanced microscopy techniques, namely atomic force, fluorescence, and holotomography microscopies (AFM, FM, and HTM, respectively) to provide further insights into the nature of the observed photoactivity of MCF-Au-L NMs. In addition, in situ radiation, using a modified HTM microscope with an IR laser accessory, demonstrates the photoactivity of the MCF-Au NMs and their suitability for destroying cancerous cells through photodynamic therapy. The combined imaging capabilities demonstrate clear morphological changes, NMs internalization, and oxidative damage. Our results confirm that the fabricated multifunctional NMs exhibit high stability in aqueous solution, chemical solidity, superparamagnetic behavior, and effective IR responses, making them promising precursors for hybrid cancer therapy.

Several chronic inflammatory processes are currently being studied in relation to other systems to better understand the regulation mechanisms and identify potential therapeutic targets. A significant body of evidence supports the role of the nervous system in regulating various immunological processes. This study investigates the relationship between pterygia and the sympathetic nervous system, focusing on their interaction in the inflammatory response and fibrogenic process. Sixteen surgical specimens of primary pterygia and four conjunctival tissue samples were examined, and their morphology was analyzed using hematoxylin–eosin and Masson’s trichrome stains. The gene expression of adrenergic receptors, as well as inflammatory and fibrogenic cytokines, was also assessed. Additionally, both adrenergic receptors and tyrosine hydroxylase were found to be localized within the tissues according to immunohistochemistry and immunofluorescence techniques. Increased expression of proinflammatory, fibrogenic, and adrenergic genes was observed in the pterygium compared to the healthy conjunctiva. Adrenergic receptors and tyrosine hydroxylase were localized in the basal region of the epithelium and within blood vessels, closely associated with immune cells. Neuroimmunomodulation plays a key role in the pathogenesis of pterygia by activating the sympathetic nervous system. At the intravascular level, norepinephrine promotes the migration of immune cells, thereby sustaining inflammation. Additionally, sympathetic nerve fibers located at the subepithelial level contribute to epithelial growth and the fibrosis associated with pterygia.