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International Journal of Molecular Sciences

International Journal of Molecular Sciences is an international, peer-reviewed, open access journal providing an advanced forum for biochemistry, molecular and cell biology, molecular biophysics, molecular medicine, and all aspects of molecular research in chemistry, and is published semimonthly online by MDPI.
The Australian Society of Plant Scientists (ASPS)Epigenetics Society, European Chitin Society (EUCHIS), Spanish Society for Cell Biology (SEBC) and others are affiliated with IJMS and their members receive a discount on the article processing charges.
Indexed in PubMed | Quartile Ranking JCR - Q1 (Biochemistry and Molecular Biology)

All Articles (103,934)

Kaposi sarcoma (KS) is an intermediate-grade vascular tumour that has undergone major treatment and diagnostic breakthroughs following the discovery of Human herpesvirus 8 (HHV8). Whilst classically described in Eastern European populations, the endemic and epidemic forms of KS have facilitated its association with AIDS. This was led by the detection of HHV8 by PCR, and thereafter, immunohistochemically. This not only enabled the recognition and diagnosis of complex histopathological KS subtypes but also facilitated distinction from its mimickers, including acroangiodermatitis and pyogenic granuloma. Recent advances in the viral genomics of HHV8 have expanded the diagnostic landscape of KS clinically and molecularly. The latent phase of replication in the HHV8 lifecycle reveals numerous angiogenic and inflammatory factors. Novel therapies targeting these viral–human molecular interactions may prove useful. However, this is highly dependent on the clonal nature of KS. Conflicting research outcomes demonstrate varying viewpoints on the clonal (monoclonal/oligoclonal/polyclonal) nature of KS, heightening the tumoural versus inflammatory pseudoneoplastic controversy. Understanding the clinical context of KS is fundamental to understanding its clonality, and a dearth of this clinical information in recent studies appears to be the critical factor in determining the true clonal nature of KS. The current molecular landscape, histopathology, treatment options, and opinions on clonality are critically reviewed.

16 October 2025

Timeline of the key discoveries in KS. Key: KS—ARTs—antiretroviral therapies, IHC—immunohistochemistry, PCR—polymerase chain reaction. Created in BioRender. https://BioRender.com/6zob4su (accessed on 11 August 2025).

Furfural and 5-hydroxymethylfurfural are considered as essential platform molecules for the chemical industry, acting as precursors and intermediates of numerous products. They are produced from pentoses and hexoses, respectively, in an acid medium. In this work, biomass from a green macroalgae, Ulva rigida, was treated under acidic conditions provided by heterogeneous catalysts in order to promote the dehydration of its monosaccharides into furfural and 5-hydroxymethylfurfural. Particularly, two functionalized mesoporous silicas, HMS and SBA-supported metal oxides (Nb2O5 and ZrO2), were used as catalysts. Their textural, structural, and acid properties were deeply studied, providing excellent BET surface areas (ranging 424 to 1204 m2/g) and a high concentration of acid sites (220–460 µmol/g), which then translated into great catalytic performances (77.8% and 64.1% of furfural and HMF molar yields, respectively, using HMS-Nb) after a 4 h of reaction time at 180 and 160 °C, respectively. The catalyst showed excellent stability and recyclability as it could be reused for up to five reaction runs with only a slight decrease in performance.

15 October 2025

N2 adsorption-desorption isotherms of (A) HMS-NbZr, (B) HMS-Nb, (C) HMS-Zr, (D) SBA-NbZr, (E) SBA-Nb, and (F) SBA-Zr.

Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are rare, autosomal dominant skeletal dysplasias characterised by disproportionate short stature, joint deformities, and early-onset osteoarthritis. These conditions result from mutations in key cartilage extracellular matrix (ECM) components, including cartilage oligomeric matrix protein (COMP), matrilin-3, and type IX collagen. Although genetically and clinically heterogeneous, PSACH and MED share convergent pathogenic mechanisms. Misfolded mutant ECM proteins are retained within the endoplasmic reticulum (ER) of growth plate chondrocytes, triggering chronic ER stress and impairing chondrocyte proliferation, differentiation, and survival. Moreover, some of the mutant protein is secreted and incorporated into the matrix, leading to altered collagen fibrillogenesis, disrupted proteoglycan distribution, and compromised biomechanical integrity. These alterations extend beyond cartilage, impacting tendons, ligaments, and muscle–tendon junctions, contributing to joint laxity, impaired force transmission, and mild myopathy. This review discusses the structural and functional consequences of ECM disorganisation in PSACH and MED, highlighting its central role in disease progression and emphasising the importance of considering ECM abnormalities when developing therapeutic strategies for rare short stature-associated skeletal disorders.

15 October 2025

Disease mechanisms associated with PSACH-MED: COMP, matrilin-3, and collagen IX mutations. (A) The epiphyseal growth plate contains of a single cell type, chondrocytes, which are organised into distinct zones according to their differentiation status. (B) Proliferating chondrocytes secrete COMP, matrilin-3, and collagen IX, which interact to organise and stabilise the cartilage extracellular matrix. (C) PSACH-MED disease-causing mutations in these genes disrupt both intracellular homeostasis and cartilage extracellular matrix organisation. Exon-skipping mutations in the COL3 domain of collagen IX, currently being modelled in mice, are anticipated to compromise extracellular matrix assembly; however, their intracellular effects remain unknown. Matrilin-3 missense mutations within the vWFA domain lead to the intracellular retention of the mutant protein and the activation of a pathological UPR, with downstream effects on chondrocyte proliferation and apoptosis. In addition, loss of its linker function disrupts extracellular matrix organisation. COMP mutations have domain-specific effects: T3 mutations cause protein retention, triggering non-canonical ER stress and oxidative stress that disrupt both chondrocyte function and the extracellular matrix, whereas CTD mutations permit secretion of mutant COMP, triggering a mild UPR, with downstream consequences for intracellular function and matrix organisation. Overall, these mutations exert both intracellular and extracellular effects, highlighting their dual impact on chondrocyte biology and extracellular matrix integrity. (RZ = resting zone, PZ = proliferative zone, HZ = hypertrophic zone, COL = collagenous, NC = non-collagenous, vWFA = von Willebrand factor A, ER = endoplasmic reticulum, UPR = unfolded protein response, EGF = epidermal growth factor, T3 = Type III, and CTD = C-terminal domain).

Portulaca oleracea Extract Modulates Diet-Dependent Neuroplasticity in a Murine Model of MCD-Induced NAFLD and Depression

  • Smaranda Ioana Mitran,
  • Mădălina Iuliana Muşat and
  • Cornelia Bejenaru
  • + 9 authors

Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a systemic condition with neuropsychiatric comorbidities, including depression. Growing evidence for the neuroprotective, antidepressant, and anxiolytic potential of Portulaca oleracea (PO) extract, provides a compelling rationale for investigating its effects in the interaction between dietary models of NAFLD and vulnerability to stress-related disorders. Fifty-four 14- to 18-week-old male and female C57BL/6N mice were distributed in two equal groups and fed either a methionine- and choline-deficient diet (MCD) or a methionine- and choline-controlled diet (MC). Subsequently, half of each group was subjected to chronic unpredictable mild stress (CUMS) and PO treatment. MCD caused significant weight loss, whereas MC promoted weight gain. Behaviorally, MCD induced anhedonia- and anxiety-like behaviors, worsened by CUMS. MC diet reduced CUMS-induced anhedonia, though anxiety-like behavior emerged only under stress. Recognition memory was impaired in stressed MCD-fed mice, while MC-fed mice showed enhanced novel object preference. At the cellular level, MCD suppressed hippocampal microglia and caused cortical astrocyte dysfunction, whereas the MC diet promoted cortical neurogenesis potentiated through PO, abolished by chronic stress. These findings underscore the impact of dietary composition on PO’s systemic effects under chronic stress and support a mechanistic link between NAFLD-related dysfunction and depression-like phenotypes.

15 October 2025

(a) Body weight evolution during the experiment. Anhedonia-like behavior assessed by Sucrose Preference Test in mice which were fed (b) MCD or (c) MC diet. (d) Diet-dependent comparison of percent change in sucrose preference. The plots show mean values ± SD, * p < 0.05, ** p < 0.01. CUMS: Chronic unpredictable mild stress; MC: Methionine- and choline-controlled diet; MCD: Methionine- and choline-deficient diet; PO: Portulaca oleracea; SD: Standard deviation; VEH: Vehicle.

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International Journal of Molecular Sciences - ISSN 1422-0067Creative Common CC BY license