Search Results (130)

Heat stress negatively affects bovine fertility and embryonic development, while cryopreservation imposes additional cellular stress that may impair embryo survival. The present study investigated whether controlled heat treatment applied during the early morula stage could influence subsequent blastocyst development, molecular stress responses, and post-thaw survival of bovine embryos. In vitro-produced bovine embryos were exposed to controlled thermal treatment involving gradual elevation in temperature from 38.8 °C to 40.0 °C followed by subsequent cooling. Blastocyst formation, post-thaw survival after slow freezing, and the expression of stress-associated genes and microRNAs were evaluated. Heat treatment did not significantly affect blastocyst formation rates or post-thaw embryo survival compared to the control groups. However, significant alterations in the expression of stress-associated markers were observed. The expression of HSP90AA1 and HSPB11 was significantly reduced following heat treatment, while cryopreservation induced increased expression of these markers compared to embryos exposed only to heat treatment. Significant alterations were also detected in the expression of several stress-associated microRNAs. These findings suggest that controlled heat exposure during the morula stage may induce molecular changes associated with the embryonic response to heat stress without compromising developmental competence or cryosurvival. The results contribute to a better understanding of the molecular mechanisms underlying embryonic responses to thermal and cryogenic stress and may support future optimization of embryo production and cryopreservation strategies. Full article

Background: Cerebral venous sinus thrombosis (CVST) is a critical cause of brain injury and intracranial hypertension. However, its underlying molecular mechanisms remain poorly understood, limiting the development of targeted therapies. This study aims to systematically identify key molecular targets and signaling pathways involved in CVST-induced brain lesions using multi-omics approaches in a modified rat model of CVST. Methods: An optimized rat CVST model was established. Cortical tissues were collected from Sham-operated, 2-day post-CVST, and 7-day post-CVST groups for transcriptomic, proteomic, and single-cell transcriptomic sequencing. Bioinformatics analyses were performed to identify differentially expressed genes/proteins, followed by functional enrichment, protein–protein interaction network construction, and hub-gene screening. Further investigations included drug enrichment analysis, molecular docking, and molecular dynamics, as well as the prediction of competing endogenous RNA networks, transcription factor analysis, and expression profiling of potential edema-related therapeutic targets. Results: Multi-omics analyses revealed dynamic changes in gene and protein expression in the brain after CVST, along with associated pathways involved in immune inflammatory responses and tissue repair. Integrative analysis identified 12 core genes (Cd44, Cd40, Sdc1, Myd88, Icam1, Stat3, Jak2, Ptgs2, Aldh1a1, Hspb1, Pxdn, and Casp3). Single-cell RNA sequencing validated their expression and delineated cell-type specificity. Molecular docking hinted at the high binding potential of glucocorticoids such as dexamethasone and methylprednisolone to several core targets (JAK2, PTGS2, and CD44), with all docked complexes showing binding energies below −8.2 kcal/mol. Further molecular dynamics simulations indicated that methylprednisolone forms a stable complex with CD44, driven primarily by van der Waals and electrostatic interactions. Additionally, dynamic levels of several potential edema-related targets (Kcnn4, Piezo1, Trpv4, and Atp1a2) were observed. Conclusions: In summary, by applying integrated multi-omics profiling to a modified rat model, this study systematically mapped the molecular landscape of CVST-induced brain injury. A number of candidate targets and signaling pathways emerged from our analysis, along with several compounds of potential therapeutic interest. Collectively, these results provide a basis for further investigation into the mechanisms underlying CVST and for the design of novel treatment approaches. Full article

The small heat shock protein HSPB1 is a ubiquitously expressed mechanoresponsive chaperone essential for cytoskeletal remodeling under mechanical load. Mutations in HSPB1, including S135F, cause Charcot-Marie-Tooth (CMT) peripheral neuropathy, yet the mechanisms underlying the selective vulnerability of peripheral nerves remain enigmatic. Here we demonstrate that substrate stiffness is a critical determinant of HSPB1^S135F-mediated neurodegeneration. Using stiffness-tunable polydimethylsiloxane (PDMS) substrates (1 kPa, 10 kPa, 2 MPa) and uniaxial cyclic stretch, we show that primary dorsal root ganglia (DRG) neurons and SH-SY5Y cells expressing HSPB1^S135F exhibit profound deficits in mechanoadaptation. On compliant substrates (10 kPa), HSPB1^S135F causes stretch-induced axon fragmentation and neuronal death, whereas HSPB1^WT confers robust neuroprotection. HSPB1^S135F also disrupts stiffness-directed neuritogenesis in differentiated SH-SY5Y cells: HSPB1^WT-expressing cells show optimal axonal outgrowth and βIII-tubulin expression on 10 kPa substrates mimicking muscle tissue stiffness, while HSPB1^S135F mutants display disorganized focal adhesions and complete differentiation failure. Mechanistically, we uncover that HSPB1^S135F dysregulates stage-specific transglutaminase (TGase) expression—insufficient TGase during early neuritogenesis impairs filopodia stabilization, whereas aberrant TGase persistence at late stages constrains axon extension. Our findings establish HSPB1 as a biomechanical sensor that integrates ECM stiffness signals to coordinate peripheral nerve regeneration, and identify defective mechanoadaptation as a previously unrecognized pathomechanism in CMT. These results open new avenues for stiffness-targeted therapeutic strategies in peripheral neuropathy. Full article

Background: HCC remains one of the leading causes of cancer-related mortality worldwide, and the therapeutic efficacy of sorafenib is limited by the development of acquired resistance. Increasing evidence indicates that the tumor microenvironment, particularly HSCs, plays a pivotal role in modulating drug response; however, the underlying molecular mechanisms remain incompletely elucidated. Methods: Co-culture systems, mouse models, and biochemical assays were employed to evaluate the effects of HSCs on sorafenib sensitivity and ferroptosis in HCC cells. Transcriptomic analyses of data from The Cancer Genome Atlas were performed to identify key long non-coding RNAs (lncRNAs), followed by gain- and loss-of-function experiments to determine their biological roles. The underlying molecular mechanisms were further investigated through expression profiling, correlation analyses, and RNA stability assays. Results: HSCs markedly reduced the sensitivity of HCC cells to sorafenib by inhibiting ferroptosis, as evidenced by decreased levels of ferrous iron, reactive oxygen species, and lipid peroxidation, accompanied by increased glutathione content and activation of the NRF2 signaling pathway. LINC00152 was identified as a critical lncRNA that was upregulated in both HCC tissues and HCC cells co-cultured with HSCs, and its high expression was associated with poor prognosis. Functional studies demonstrated that LINC00152 promoted sorafenib resistance and suppressed ferroptosis both in vitro and in vivo. Mechanistically, LINC00152 enhanced HSPB1 expression by stabilizing its mRNA. Notably, HSPB1 knockdown reversed the effects of LINC00152, restoring ferroptosis and drug sensitivity to sorafenib. Conclusions: These findings reveal a novel HSCs–LINC00152–HSPB1 axis that promotes ferroptosis resistance and sorafenib tolerance in HCC. Targeting this pathway may represent a promising therapeutic strategy for overcoming drug resistance and improving clinical outcomes in patients with HCC. Full article

Apoptosis maintains tissue homeostasis, and its dysregulation is closely associated with breast cancer progression and therapeutic resistance. We performed an integrative analysis of apoptosis-related signaling in breast cancer tissues across five molecular subtypes and compared these patterns with systemic apoptotic responses following cryoablation of benign fibroadenomas. Gene expression profiling was conducted using mRNA microarrays and validated by qRT-PCR and ELISA. Apoptosis pathway activity was assessed with the MSigDB HALLMARK_APOPTOSIS gene set, including intrinsic and extrinsic pathway scoring and an apoptotic balance index (ABI). MicroRNA profiling combined with in silico analyses identified potential miRNA–mRNA interactions. A progressive shift toward reduced pro-apoptotic and enhanced stress-adaptive signaling was observed with increasing tumor aggressiveness, most pronounced in triple-negative and non-luminal HER2-positive cancers. This pattern included reduced intrinsic pathway activity, decreased ABI, downregulation of pro-apoptotic genes (BIK, BMF, TXNIP), and upregulation of stress-associated or cytoprotective genes (HSPB1, PPT1). Several expression patterns were accompanied by overexpression of miRNAs (miR-582-5p, miR-421, miR-106b-5p, miR-20a-5p, miR-20b-5p, miR-93-5p) predicted to target apoptosis-related genes. In contrast, fibroadenoma cryoablation was associated with transient systemic modulation of apoptosis-related genes and proteins followed by gradual normalization. These findings highlight differences between apoptosis-related dysregulation in malignant tissue and regulated systemic responses following benign tissue injury, supporting pathway-level interpretation and identifying candidate molecular networks warranting further mechanistic and translational investigation. Full article

Radiation-induced trismus (RIT) is a common and function-limiting late complication of radiotherapy for head and neck cancers, particularly when the masticatory muscles and temporomandibular joint receive high doses. Despite advances in intensity-modulated radiotherapy, RIT remains a significant survivorship problem, and robust biological biomarkers capable of predicting individual susceptibility are lacking. Heat shock protein 27 (HSP27; HSPB1) is a small heat shock protein that regulates multiple cellular stress responses, including proteostasis, cytoskeletal dynamics, redox homeostasis, apoptosis, and inflammatory signaling. In head and neck malignancies, HSP27 overexpression has been associated with treatment resistance and fibrosis-prone tissue remodeling. Experimental studies further demonstrate that HSP27 promotes transforming growth factor-β-mediated myofibroblast differentiation and extracellular matrix deposition, whereas pharmacologic or genetic inhibition attenuates radiation- or bleomycin-induced pulmonary fibrosis in vivo. Evidence from skeletal muscle biology also indicates that HSP27 modulates muscle integrity, denervation-associated atrophy, inflammatory signaling, and cytoskeletal stability. Although HSP27 has been widely investigated in radiation responses, fibrosis, and skeletal muscle stress adaptation, its potential involvement in the pathogenesis of RIT has not been systematically examined. This review proposes a conceptual framework in which HSP27 functions as an integrative molecular mediator linking radiation-induced oxidative stress, endothelial injury, and fibro-atrophic remodeling within the masticatory apparatus. By integrating current evidence on the epidemiology, dosimetric determinants, imaging correlates, and pathophysiology of RIT with the structural and functional biology of HSP27, this review provides the first tissue-specific synthesis of molecular stress signaling and clinical mechanisms relevant to RIT susceptibility. We further suggest that HSP27 signaling may influence susceptibility to fibro-neuromuscular injury in irradiated masticatory tissues. Given the absence of direct experimental or clinical evidence in this setting, these considerations are derived from mechanistic convergence across related biological systems and should be interpreted as biologically plausible but unproven, with potential implications for future biomarker development and biologically informed prevention strategies. Full article

Fish oil (FO) has been shown to confer beneficial effects on hepatic diseases in both humans and animals. This study aimed to investigate whether dietary fish oil (FO) supplementation alleviates deoxynivalenol (DON)-induced liver injury by modulating the ferroptosis signaling pathway in weaned piglets. Twenty-four weaned piglets were allocated to a 2 × 2 factorial design, with the main factors consisting of dietary treatment (5% corn oil or 5% FO supplementation) and DON exposure (basal diet or diet contaminated with 4 mg/kg DON). After 21 days of dietary treatment, piglets were euthanized for collection of blood and liver samples. Dietary FO significantly attenuated DON-induced hepatic structural damage and inflammatory infiltration. Specifically, FO supplementation reduced the activities of aspartate transaminase (AST) and alkaline phosphatase (ALP), as well as the AST/alanine aminotransferase (ALT) ratio following DON exposure. Dietary FO also decreased malondialdehyde (MDA) concentrations in both the liver and serum, lowered hepatic 4-hydroxynonenal (4-HNE) level and Fe²⁺ content, and increased hepatic glutathione (GSH) content. Moreover, dietary FO ameliorated ultrastructural liver damage induced by DON. Furthermore, DON significantly downregulated the mRNA levels of multiple genes associated with iron metabolism and ferroptosis, including heat shock protein beta-1 (HSPB1), acyl-CoA synthetase long chain family member 4 (ACSL4), and arachidonate 15-lipoxygenase (ALOX15), and upregulated the mRNA levels of transferrin (TF), ferritin heavy chain (FTH), solute carrier family 7 member 11 (SLC7A11), and transferrin receptor 1 (TFR1). Dietary FO counteracted these alterations by decreasing the mRNA of SLC7A11, TFR1, FTH, and TF after DON exposure. Finally, FO significantly decreased the protein expression of SLC7A11, iron-responsive element-binding protein 2 (IREB2), and FHT1 and increased the GPX4 protein expression following DON exposure. These findings suggest that FO may ameliorate DON-induced liver injury in weaned piglets, possibly through suppressing the ferroptosis signaling pathway. Full article

Charcot–Marie–Tooth (CMT) disease represents the most prevalent inherited peripheral neuropathy with a broad range of clinical manifestations, inheritance patterns, and causative genes. The primary pathological hallmark is progressive degeneration, predominantly affecting sensory and motor neurons, leading to prominent sensory deficits and progressive motor impairments. While neuropathy-causing mutations in the ubiquitously expressed small heat shock protein HSPB1 account for a subset of axonal CMT cases, the mechanisms underlying the selective vulnerability of peripheral neurons remain poorly understood. In this review, we synthesize emerging evidence to reframe HSPB1-related CMT as a prototypical gene–environment interaction disorder. The unique anatomical exposure and high metabolic demands of the peripheral nervous system (PNS) render it particularly vulnerable to HSPB1 mutation-mediated homeostatic collapse, which manifests through three interconnected pathological axes: proteostatic disturbance, cytoskeletal dysregulation, and mitochondrial dysfunction. Crucially, these deficits converge to impair the stress adaptability of peripheral neurons, creating a maladaptive feedback loop wherein environmental stressors exacerbate intrinsic vulnerabilities. We further propose a phase-specific therapeutic framework that prioritizes early intervention during the clinically silent yet biologically active prodromal stage, when targeted modulation of the HSPB1 chaperone interactome and remodeling neural homeostasis may forestall neurodegeneration. This therapeutic paradigm shift from symptomatic management to preclinical neuroprotection underscores the imperative for precision medicine approaches in future CMT intervention. Full article

Background: This study aimed to assess the effects of postbiotic derived from Bacillus subtilis natto (Szendi2020) on endothelial responses under LPS-induced inflammatory stress. Methods: In human umbilical vein endothelial cells (HUVECs), inflammation was induced with 200 ng/mL LPS. Cell viability, apoptosis, and mitochondrial integrity were assessed using MTT assay, DiIC, and Sytox Green permeability assays. Intracellular ROS levels, heat shock proteins (HSPB1/Hsp27, HSPA1L/Hsp70), adhesion molecules (ICAM-1, VCAM-1), tight junction protein (Occludin), transcription regulators (NF-κB, TNFα), and proinflammatory cytokines (IL-1β, IL-6, IL-8) were quantified using qPCR and ELISA. Results: LPS exposure significantly induced apoptosis in HUVECs, as reflected by decreased metabolic activity, decreased mitochondrial membrane potential, and increased cell death (p < 0.05). Concurrent postbiotic administration completely abolished LPS-induced cytotoxicity in all assay platforms, demonstrating a potent cytoprotective effect. Postbiotic treatment significantly reduced LPS-induced ROS accumulation (p < 0.05). LPS significantly increased Hsp27 and Hsp70 mRNA expression. However, combined LPS and postbiotic exposure mitigated Hsp27 and Hsp70 mRNA expression compared with LPS treatment alone (p < 0.001, p < 0.005). Postbiotic treatment also decreased the upregulation of adhesion molecules induced by LPS. Although this effect decreased after 24 h (p < 0.001). LPS strongly increased NF-κB, IL-1β and TNFα mRNA levels and was suppressed by postbiotics at early time points but not maintained over 24 h. Importantly, postbiotics significantly reduced IL-6, and IL-8 expression at both the mRNA and protein levels, highlighting the attenuation of endothelial inflammatory features (p < 0.05, p < 0.005, p < 0.001). Conclusions: Our results are the first to demonstrate that postbiotics derived from Bacillus subtilis natto (Szendi2020) exert potent cytoprotective and anti-inflammatory effects in LPS-induced endothelial inflammation. By reducing ROS accumulation, preventing apoptosis, stabilizing mitochondrial and barrier integrity, modulating HSP, NF-κB, and cytokine responses. Postbiotics may be promising therapeutic candidates for alleviating endothelial inflammation and the resulting endothelial dysfunction. Full article

Protected Designation of Origin (PDO) beef products are recognized for their higher quality, although the native breeds used often show lower productivity compared to commercial crosses. This study aimed to compare the proteome profiles of Arouquesa and crossbred beef using 2D-DIGE, and evaluating crude protein, energy, and fatty acid composition. Arouquesa beef had higher energy values (p < 0.05), whereas crossbred samples showed greater protein content (p < 0.05). Moreover, Arouquesa beef had higher proportions of microminerals, namely zinc, iron, and manganese (p < 0.05). The Arouquesa breed also presented higher proportions of most fatty acids, including saturated, monounsaturated, and polyunsaturated. Proteomic analysis identified 34 differentially abundant proteoforms from 23 proteins. In Arouquesa, proteins associated with muscle contraction (MYLPF, TNNT1), glycolysis/gluconeogenesis (TPI1, GPD1), oxygen transport (HBB, HBA), and heat shock response (CRYAB, HSPB1) were more abundant or had altered spot patterns, suggesting their roles in meat tenderness, color, and fat-related characteristics. Conversely, crossbred beef showed elevated levels of glycolytic enzymes (PGM1, ENO3, and some proteoforms of TPI1 and GPI) and structural proteins (MYL1), related with higher muscle growth and different fiber composition. The identified proteins provide possible molecular markers that distinguish Arouquesa from commercial breeds. These validated proteins in the future can support breed characterization and verification of PDO certification specifications. Full article

Mesenchymal stromal cells (MSCs) are promising therapeutic agents, largely due to their capacity for self-renewal, differentiation, and immunomodulation. Importantly, these beneficial effects are frequently mediated by the MSC secretome, which contains factors with anti-inflammatory, anti-apoptotic, and pro-regenerative properties. However, cellular senescence can impair these critical functions. To identify senescence-associated changes in the MSC secretome that may regulate aging and intercellular communication, we performed a mass spectrometry-based proteomic analysis of the conditioned medium from MSCs undergoing stress-induced senescence. Our analysis confirmed the upregulation of established aging markers, such as IL-6, PAI-1, and IGFBP7. Furthermore, we identified a significant increase in lesser-known senescence-associated secretory phenotype (SASP) components, including INHBA—a known inhibitor of proliferation—and DKK3, which blocks stromal cell pluripotency. Pathway analysis revealed that stress-induced senescence broadly affected proteins involved in glycolysis, immune response, hemostasis, and the regulation of cell death and the cell cycle. These alterations are likely to negatively impact the MSC microenvironment. Interestingly, the cellular response to senescence was dualistic. Alongside detrimental SASP factors, we observed an increase in protective proteins such as annexins (ANXA1, ANXA2), antioxidants (TXN, PRDX1, PRDX6), and the heat shock protein HSPB1, which collectively defend neighboring cells from inflammation and oxidative stress. These findings underscore the complex etiology of cellular senescence and the paradoxical nature of the SASP. The obtained data also emphasize the necessity of comprehensive proteomic profiling of the MSC secretome across different aging models to harness the full therapeutic potential of MSCs and their secretomes for regenerative medicine. Full article

Heat shock proteins (HSPs) are highly conserved molecular chaperones that play a key role in maintaining protein homeostasis, or proteostasis, especially under stressful environmental conditions such as hyperthermia, hypoxia, or the presence of reactive oxygen species. In pancreatic cancer, the expression of many HSP isoforms is dysregulated, contributing to the activation of mechanisms that promote tumor development, including proliferation, invasion, angiogenesis, treatment resistance, and cancer cachexia syndrome. HSPs are significant diagnostic and prognostic biomarkers. Some of them, such as HSP27, HSP70, and HSP90, have been shown to correlate with treatment response and patient survival. Others, including HSPA2 and HSPB6, may indicate an increased risk of disease recurrence. These proteins also represent promising therapeutic targets. Preclinical and clinical studies suggest that inhibiting HSP activity and associated signaling pathways may inhibit tumor growth and increase treatment efficacy. These therapeutic effects include inducing apoptosis, autophagy, and ferroptosis, as well as sensitizing cancer cells to chemotherapy and immunotherapy. This article summarizes the current knowledge about the role of HSPs in pancreatic cancer biology, their significance as biomarkers, and their potential therapeutic applications in treating pancreatic ductal adenocarcinoma (PDAC). Most studies conducted so far have been preclinical, and due to the promising results, further clinical investigation is warranted. Full article

An emerging challenge in prostate cancer (PCa) treatment is the development of drug cross-resistance, wherein resistance to enzalutamide (ENZ), an androgen receptor signaling inhibitor (ARSI), also confers resistance to subsequent ARSI and docetaxel (DTX) treatments. The mechanisms underlying this drug cross-resistance remain unclear. Through RNA sequencing, we identified 93 overlapping differentially expressed genes (DEGs) in ENZ- and DTX-resistant PCa cells. Among the DEGs, HSPB1, which encodes heat shock protein 27 (HSP27), emerged as a key gene of interest. HSP27 is a known target of lens epithelium-derived growth factor p75 (LEDGF/p75), a transcription coactivator regulated by glucocorticoid receptor (GR). Both GR and LEDGF/p75 are overexpressed in advanced PCa and promote drug resistance. HSP27 was overexpressed in ENZ and DTX cross-resistant PCa cell lines and its expression was decreased upon GR or LEDGF/p75 silencing. ChIP sequencing confirmed GR binding at the HSPB1 promoter. Pharmacological targeting of HSP27 in drug-resistant cells reduced proliferation, clonogenicity, and tumorsphere formation, and restored sensitivity to ENZ and DTX. Notably, high transcript expression of a GR-LEDGF/p75-HSP27 gene panel correlated with worse overall survival in PCa patients (n = 4259). These findings identified this axis as a driver of PCa drug cross-resistance and promising therapeutic target for overcoming treatment failure. Full article

(1) Background: Chronic myeloid leukemia (CML) is a myeloproliferative disorder driven by the BCR::ABL oncoprotein. During the chronic phase, Philadelphia chromosome-positive hematopoietic stem cells generate proliferative myeloid cells with various stages of maturation. Despite this expansion, leukemic stem cells (LSCs) retain self-renewal capacity via asymmetric cell divisions, sustaining the stem cell pool. Quiescent LSCs are known to be resistant to tyrosine kinase inhibitors (TKIs), potentially through BCR::ABL-independent signaling pathways. We hypothesize that dysregulation of genes governing asymmetric division in LSCs contributes to disease progression, and that their expression pattern may serve as a prognostic marker during the chronic phase of CML. (2) Methods: Genes related to asymmetric cell division in the context of hematopoietic stem cells were extracted from the PubMed database with the keyword “asymmetric hematopoietic stem cell”. The collected relative gene set was tested on two independent bulk transcriptome cohorts and the results were confirmed by single-cell RNA sequencing. (3) Results: The expression of genes involved in asymmetric hematopoietic stem cell division was found to discriminate disease phases during CML progression in the two independent transcriptome cohorts. Concordance between cohorts was observed on asymmetric molecules downregulated during blast crisis (BC) as compared to the chronic phase (CP). This downregulation during the BC phase was confirmed at single-cell level for SELL, CD63, NUMB, HK2, and LAMP2 genes. Single-cell analysis during the CP found that CD63 is associated with a poor prognosis phenotype, with the opposite prediction revealed by HK2 and NUMB expression. The single-cell trajectory reconstitution analysis in CP samples showed CD63 regulation highlighting a trajectory cluster implicating HSPB1, PIM2, ANXA5, LAMTOR1, CFL1, CD52, RAD52, MEIS1, and PDIA3, known to be implicated in hematopoietic malignancies. (4) Conclusion: Regulation of CD63, a tetraspanin involved in the asymmetric division of hematopoietic stem cells, was found to be associated with poor prognosis during CML progression and could be a potential new therapeutic target. Full article

Background: Previous proteomic studies provided valuable information about cataracts, but unclarified issues, such as sex and ethnicity-associated differences, remain. This study aimed to provide additional data on cataract-related proteins regarding age, sex, and cataract type. Methods: Twenty-six female and seven male Turkish cataract patients were screened for visual acuity and dysfunctional lens index. A nano-LC-MS/MS system and Progenesis QI software v3.0 were used for protein identification and quantification. The remaining data were evaluated with SPSS Version 29.0 software. Results: Proteins that showed age-associated changes were mainly involved in cytoskeletal organization. A glyoxalase enzyme, caveolin 1, and HS90B were lower, and RAB8B and ATP6V1B1 were higher in lenses in women. Proteins with lower levels in cataractous lenses than in transparent lenses included filensin and phakinin, concurrent with previous publications, and LCTL, GDI, HSPB1, and EIF4A2, not reported before. Corticonuclear cataracts constituted the only group showing depletions in putatively protective proteins, while the cortical type was the least influenced. ANXA1 and DNHD1 positively, and TCPD, SEC14L2, and PRPS1 proteins negatively correlated with visual acuity. Conclusions: This study revealed cataract-related proteins concurrent with earlier studies and new ones hitherto unreported. Despite the low number of patients investigated, the results merit further research, as these new proteins are highly likely to be involved in cataractogenesis. Full article