Claudins, Inflammation and Epithelial-Mesenchymal Transition in Gastric Tissue

doi:10.4172/2161-069x.1000149

Cited by 3 publications

(2 citation statements)

References 125 publications

(94 reference statements)

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“…In the lung, the disruption of claudin-18 expression stimulates pulmonary fibrosis or chronic obstructive pulmonary disease (Schlingmann et al, 2015). Furthermore, claudin modification has been established in several cancers, including gastric cancer, via the activation of epithelial-to-mesenchymal transition (EMT), a mechanism that is also involved in the progression of fibrosis (Rendon-Huerta et al, 2013).…”

Section: Claudin 34d (Cldn34d)mentioning

confidence: 99%

Recent Insights Into SREBP as a Direct Mediator of Kidney Fibrosis via Lipid-Independent Pathways

Dorotea

Koya

2020

Front. Pharmacol.

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Sterol regulatory-element binding proteins (SREBPs) are classical regulators of cellular lipid metabolism in the kidney and other tissues. SREBPs are currently recognized as versatile transcription factors involved in a myriad of cellular processes. Meanwhile, SREBPs have been recognized to mediate lipotoxicity, contributing to the progression of kidney diseases. SREBP1 has been shown to bind to the promoter region of TGFβ, a major pro-fibrotic signaling mechanism in the kidney. Conversely, TGFβ activates SREBP1 transcriptional activity suggesting a positive feedback loop of SREBP1 in TGFβ signaling. Public ChIP-seq data revealed numerous non-lipid transcriptional targets of SREBPs that plausibly play roles in progressive kidney disease and fibrosis. This review provides new insights into SREBP as a mediator of kidney fibrosis via lipid-independent pathways.

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Section: Claudin 34d (Cldn34d)mentioning

confidence: 99%

Recent Insights Into SREBP as a Direct Mediator of Kidney Fibrosis via Lipid-Independent Pathways

Dorotea

Koya

2020

Front. Pharmacol.

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“…Claudins are another class of EMT-associated proteins [89]. In FC, transmembrane tight junction protein claudin is dislocated from membrane to nucleus.…”

Section: Immunohistochemistry Of Thyroid Neoplasmsmentioning

confidence: 99%

Thyroid Nodules in Diagnostic Pathology: From Classic Concepts to Innovations

Fridrihsone¹,

Štrumfa²,

Strumfs³

et al. 2018

Histopathology - An Update

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Thyroid nodules are frequent in general population, found in 3.7-7% of people by palpation and 42-67% by ultrasonography (US). The differential diagnosis ranges from papillary (PC), follicular (FC) and medullary (MC) carcinomas to follicular adenoma (FA) and colloid goitre. Cancer risk in thyroid nodules varies: 5% in masses found by palpation, 1.6-15% by US, 3.9-11.3% by computed tomography (CT), 5-6% by magnetic resonance imaging (MRI) and 30-50% by positron emission tomography (PET). The final diagnosis depends on fine needle aspiration (FNA) findings and histopathology. The recent WHO classification (2017) is based on classic morphology, including assessment of invasion and nuclei. New entities are defined to designate tumours with doubtful invasion or controversial nuclear features. By immunohistochemistry, PC expresses HBME-1, TROP-2, CITED1 and CK19. Notably, PC can stain for CD20. MC is recognised by neuroendocrine differentiation. To distinguish FA vs. FC, evaluation of HBME-1, p27 and galectin has been suggested. Regarding miRNAs, miR-146b, miR-222, miR-221 and miR-181b are upregulated, while miR-145, miR-451, miR-613 and miR-137 are downregulated in PC. FC features downregulated miR-199a-5p and upregulated miR-197 and miR-346. In MC, miR-21 and miR-129-5p are downregulated. In addition, increased systemic inflammatory reaction can be poor prognostic factor in thyroid cancer. The aim of this chapter is to review classic and innovative histopathology of thyroid nodules for diagnostic pathology practice and research in multidisciplinary thyroid teams.

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