{
  "research": {
    "models": [
      {
        "cat": "Animal Models",
        "items": [
          "Unilateral ureteral obstruction (UUO)",
          "Ischemia-reperfusion injury (IRI)",
          "Cisplatin nephropathy",
          "Adriamycin-induced nephrosis",
          "Streptozotocin diabetic nephropathy"
        ]
      },
      {
        "cat": "Cell Biology",
        "items": [
          "Primary renal fibroblasts & tubular cells",
          "Macrophage polarization assays",
          "3D organoid culture systems",
          "Fibroblast-to-myofibroblast transition assays",
          "siRNA / CRISPR-Cas9 gene editing"
        ]
      },
      {
        "cat": "Molecular & -omics",
        "items": [
          "Single-cell RNA sequencing (scRNA-seq)",
          "Bulk RNA-seq & proteomics",
          "Chromatin immunoprecipitation (ChIP)",
          "Proximity extension assay (Olink)",
          "Second-harmonic generation (SHG) imaging"
        ]
      }
    ],
    "themes": [
      {
        "id": "matricellular",
        "color": "teal",
        "title": "Matricellular Proteins in Kidney Injury and Repair",
        "imageUrl": "/images/10d756ea-694e-469d-b15a-6bb03944058d.png",
        "keywords": [
          "SMOC2",
          "MGP",
          "Osteopontin",
          "Periostin",
          "CCN2/CTGF",
          "Tenascin-C",
          "TGF-β signaling",
          "Integrin signaling"
        ],
        "mainText": "Matricellular proteins are a family of secreted, non-structural extracellular matrix (ECM) glycoproteins that modulate cell-ECM interactions during tissue injury, inflammation, and repair. Unlike structural matrix components such as collagens and fibronectin, matricellular proteins do not provide tensile support but instead act as context-dependent regulators of cell signaling and behavior.\n\nOur laboratory focuses on several key matricellular proteins in the kidney, including SPARC (Secreted Protein Acidic and Rich in Cysteine), osteopontin (OPN), periostin, tenascin-C, and members of the CCN family (CTGF/CCN2, CYR61/CCN1). We investigate how these proteins are regulated in response to injury stimuli such as TGF-β1, how they signal through integrins and cell surface receptors, and how they modulate the activation of downstream pro-fibrotic pathways.\n\nUsing gain- and loss-of-function approaches in cell culture systems and transgenic mouse models, we have demonstrated essential roles for SPARC in collagen deposition and fibroblast activation in the injured kidney. Current projects explore SPARC's interaction with TGF-β receptors, its regulation of SMAD and non-SMAD signaling cascades, and its potential as a therapeutic target."
      },
      {
        "id": "fibrosis",
        "color": "blue",
        "title": "Fibrosis, Extracellular Matrix Remodeling, and Chronic Kidney Disease",
        "imageUrl": "/images/e12faea3-9c97-40f7-a9f5-050441c7b81b.png",
        "keywords": [
          "ECM Remodeling",
          "Collagen deposition",
          "MMP/TIMP balance",
          "UUO model",
          "Myofibroblasts",
          "TGF-β1/SMAD3",
          "Second-harmonic generation"
        ],
        "mainText": "Renal fibrosis — characterized by progressive accumulation of ECM proteins within the glomerular, tubulo-interstitial, and vascular compartments — is the common final pathway of virtually all forms of chronic kidney disease (CKD). The resulting structural remodeling leads to loss of functional nephrons, decline of glomerular filtration, and, ultimately, end-stage renal disease.\n\nOur laboratory employs the unilateral ureteral obstruction (UUO) mouse model, a well-established and reproducible model of progressive renal fibrosis, as well as ischemia-reperfusion injury (IRI) and cisplatin-induced nephropathy models. We characterize ECM composition changes using quantitative proteomics, second-harmonic generation (SHG) microscopy, and Masson's trichrome and picrosirius red histology.\n\nA major focus is the dysregulation of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), which normally maintain ECM homeostasis. We examine how pathological shifts in MMP/TIMP balance perpetuate collagen accumulation and how matricellular proteins modulate this balance. We are also investigating how altered mechanical properties of the fibrotic matrix create a positive feedback loop that sustains myofibroblast activation."
      },
      {
        "id": "phenotypes",
        "color": "purple",
        "title": "Pathogenic Cell Phenotypes in Fibrosis",
        "imageUrl": "/images/f057b391-ab8f-490a-97d3-2d87993aa903.png",
        "keywords": [
          "Epithelial-mesenchymal transition (EMT)",
          "Macrophage polarization",
          "Pericyte-to-myofibroblast transition",
          "Cellular plasticity",
          "scRNA-seq",
          "Fibroblast activation",
          "Capillary rarefaction"
        ],
        "mainText": "Renal fibrosis is a multi-cellular process. While activated myofibroblasts are the primary producers of excess ECM, pathogenic phenotypic transitions in several other cell types amplify the fibrotic response. Our laboratory takes an integrated approach, studying these cellular actors in parallel to understand the coordinated pathobiology of CKD.\n\nIn tubular epithelial cells, we investigate epithelial-to-mesenchymal transition (EMT) — a plasticity program by which injured tubular cells acquire mesenchymal characteristics, secrete pro-fibrotic cytokines, and lose their regenerative capacity. We study how matricellular proteins drive this process and how to reverse it therapeutically.\n\nIn immune cells, we characterize macrophage polarization states in fibrotic kidneys, focusing on how M2-skewed macrophages sustain fibroblast activation through cytokine secretion and matricellular protein production. In vascular and pericyte compartments, we examine pericyte-to-myofibroblast transition (PMT) and its role in capillary rarefaction and CKD vascular pathology. Single-cell RNA sequencing (scRNA-seq) is increasingly central to our phenotyping efforts."
      },
      {
        "id": "translational",
        "color": "amber",
        "title": "Translational Approaches, Biomarkers, and Therapeutic Targeting",
        "imageUrl": "/images/8b3f0aba-6794-4735-b046-1d0815651c09.png",
        "keywords": [
          "Biomarker discovery",
          "SMOC2 in human CKD",
          "Olink proteomics",
          "Antisense oligonucleotides",
          "Small-molecule inhibitors",
          "CKD patient cohorts",
          "IgA nephropathy"
        ],
        "mainText": "Translating our mechanistic discoveries into clinically relevant insights is a central mission of the Gerarduzzi Lab. We are actively engaged in identifying urinary and serum biomarkers of renal fibrosis severity — molecules that could stratify patients by disease progression risk, guide therapeutic decisions, and serve as surrogate endpoints in clinical trials.\n\nOur current translational pipeline includes validation of candidate matricellular protein biomarkers (SPARC, periostin, osteopontin) in human CKD cohorts and in biobanked samples from patients with IgA nephropathy, focal segmental glomerulosclerosis, and diabetic nephropathy. We use ELISA, Luminex multiplex immunoassays, and proximity extension assays (Olink) to quantify these targets.\n\nOn the therapeutic side, we are exploring antisense oligonucleotide (ASO)-based and small-molecule approaches to suppress SPARC expression and disrupt its interaction with TGF-β receptors. We are also interested in re-purposing existing drugs (nintedanib, pirfenidone) and evaluating their effects on renal matricellular protein expression in our preclinical models."
      }
    ],
    "pageIntro": "Our laboratory investigates the molecular and cellular mechanisms that drive kidney fibrosis, with a focus on matricellular proteins as master regulators of tissue remodeling in chronic kidney disease.",
    "pageTitle": "Research"
  },
  "hmr": {
    "stats": [
      {
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        "value": "4"
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        "label": "Researchers",
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    ],
    "navLabel": "HMR Website",
    "pageIntro": "The Gerarduzzi Laboratory is affiliated with the Centre de recherche de l'Hôpital Maisonneuve-Rosemont (CRHMR), one of Québec's leading clinical and biomedical research institutes.",
    "pageTitle": "HMR Research Centre",
    "aboutTitle": "About the Research Centre",
    "relatedLinks": [
      {
        "desc": "Dr. Gerarduzzi's institutional profile.",
        "href": "https://crhmr.ciusss-estmtl.gouv.qc.ca/en/researcher/casimiro-gerarduzzi",
        "label": "Visit CIUSSS-EST",
        "title": "Centre intégré universitaire de santé et de services sociaux de l'Est-de-l'Île-de-Montréal"
      },
      {
        "desc": " The clinical nephrology program that partners with the Gerarduzzi Lab on translational research.",
        "href": " https://crhmr.ciusss-estmtl.gouv.qc.ca/en/research/research-axes/nephrology",
        "label": "Nephrology Program",
        "title": "Nephrology Division — HMR"
      },
      {
        "desc": "Dr. Gerarduzzi's departmental profile and teaching activities.",
        "href": "https://recherche.umontreal.ca/english/our-researchers/professors-directory/researcher/is/in30438/",
        "label": "Visit UdeM",
        "title": "Université de Montréal — Faculty of Medicine"
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    ],
    "mainCardTitle": "Hôpital Maisonneuve-Rosemont",
    "aboutParagraphs": [
      "The entre de recherche de l'Hôpital Maisonneuve-Rosemont (CRHMR) is one of Québec's most dynamic translational research environments. Located within Hôpital Maisonneuve-Rosemont, a major centre and specialty hospital in the east of Montréal, the centre benefits from direct access to clinical infrastructure, biobank resources, and multidisciplinary clinical teams.",
      "Research at the CRHMR is organized around several priority axes, including injury and critical care, kidney health, immunology, cancer, and ophthalmology disease biology. The Gerarduzzi Laboratory contributes to the renal and cardiovascular axis, bridging basic fibrosis biology with clinical nephrology.",
      "Trainees in the Gerarduzzi Lab benefit from access to core facilities at the CRHMR, including imaging platforms, genomics resources, and biobanked clinical samples, as well as training opportunities within the Université de Montréal doctoral programs in Biochemistry, Molecular Biology, and Physiology."
    ],
    "mainCardButtonUrl": "https://crhmr.ciusss-estmtl.gouv.qc.ca/fr",
    "mainCardButtonText": "Visit HMR Research Centre",
    "mainCardDescription": "The CRHMR is a recognized research centre affiliated with the Université de Montréal. It hosts over 42 researchers, clinician-scientists, and trainees working across nephrology, immunology, cancer, and ophthalmology disease research themes."
  },
  "home": {
    "ctaTitle": "Interested in Joining the Lab?",
    "heroLabel": "Gerarduzzi Lab — Université de Montréal",
    "heroTitle": "Understanding the Molecular Basis of",
    "researchAreas": [
      {
        "desc": "SMOC2, MGP, SPARC, osteopontin, periostin, CCN proteins — how these non-structural ECM components orchestrate kidney injury and repair responses.",
        "title": "Matricellular Proteins"
      },
      {
        "desc": "Mechanisms of excessive collagen deposition, matrix metalloproteinase dysregulation, and TGF-β1 signaling in chronic fibrosis.",
        "title": "ECM Remodeling & CKD"
      },
      {
        "desc": "Characterizing pro-fibrotic phenotypes in fibroblasts, tubular epithelial cells, macrophages, pericytes, and vascular cells.",
        "title": "Pathogenic Cell Phenotypes"
      },
      {
        "desc": "Identifying serum and urine biomarkers and testing novel therapeutic strategies that target matricellular signaling in CKD.",
        "title": "Translational Approaches"
      }
    ],
    "ctaDescription": "We welcome motivated postdoctoral fellows, graduate students, and undergraduate trainees who are passionate about kidney biology and fibrosis research.",
    "heroDescription": "The Gerarduzzi Laboratory investigates how matricellular proteins, extracellular matrix remodeling, and pathogenic cellular phenotypes drive the progression of chronic kidney disease and kidney cancer — with the goal of identifying novel therapeutic targets.",
    "heroTitleAccent": "Kidney Fibrosis and Cancer",
    "primaryButtonHref": "/research",
    "primaryButtonText": "Explore Our Research",
    "researchSectionDesc": "Our work spans from molecular mechanisms to translational biomarkers, always with an eye toward therapeutic impact.",
    "secondaryButtonHref": "/positions",
    "secondaryButtonText": "Join the Lab",
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    "ctaPrimaryButtonText": "View Open Positions",
    "researchSectionTitle": "Research Focus Areas",
    "ctaSecondaryButtonHref": "/contact",
    "ctaSecondaryButtonText": "Contact Us"
  },
  "contactLocation": {
    "institution": "Centre de recherche de l'Hôpital Maisonneuve-Rosemont",
    "addressLines": [
      "5345 boulevard de l'Assomption",
      "Montréal, QC, Canada, H1T 4B3"
    ],
    "latitude": 45.57312,
    "longitude": -73.55764,
    "directionsUrl": "https://www.google.com/maps/search/?api=1&query=5345+boulevard+de+l%27Assomption+Montr%C3%A9al+QC+H1T+4B3"
  },
  "pageBanners": {
    "members": {
      "intro": "Our team brings together scientists at all career stages, united by a passion for understanding kidney disease and developing better treatments for patients."
    },
    "lab-life": {
      "intro": "A look at our team, events, conferences, celebrations, and everyday life in the Gerarduzzi Lab."
    },
    "news": {
      "intro": "Lab announcements, awards, publications, conference presentations, graduations, and more from the Gerarduzzi Lab."
    },
    "positions": {
      "intro": "We are always looking for talented, motivated individuals who are passionate about kidney biology and fibrosis research to join our team."
    },
    "publications": {
      "intro": "Peer-reviewed articles, reviews, and book chapters from the Gerarduzzi Laboratory — automatically synced from PubMed."
    },
    "contact": {
      "intro": "We welcome inquiries from prospective trainees, collaborators, clinicians, and members of the media. Use the form below or reach us directly."
    }
  }
}