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MYOFIBROBLASTS HINDER RECOVERY OF HASHIMOTO THYROIDITIS IN THE ULTRASTRUCTURAL LEVEL.肌成纤维细胞在超微结构水平上阻碍桥本甲状腺炎的恢复。
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Global prevalence and epidemiological trends of Hashimoto's thyroiditis in adults: A systematic review and meta-analysis.全球成人桥本甲状腺炎的患病率和流行病学趋势:系统评价和荟萃分析。
Front Public Health. 2022 Oct 13;10:1020709. doi: 10.3389/fpubh.2022.1020709. eCollection 2022.
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Oxidative stress in Hashimoto's thyroiditis: possible adjuvant therapies to attenuate deleterious effects.桥本甲状腺炎中的氧化应激:减轻有害影响的可能辅助治疗方法。
Mol Cell Biochem. 2023 Apr;478(4):949-966. doi: 10.1007/s11010-022-04564-4. Epub 2022 Sep 27.
3
Restoration of euthyroidism with levothyroxine: implications of etiology of hypothyroidism and the degree of residual endogenous thyroid function.用左甲状腺素恢复甲状腺功能正常:甲状腺功能减退症病因和残留内源性甲状腺功能程度的影响。
Front Endocrinol (Lausanne). 2022 Jul 22;13:934003. doi: 10.3389/fendo.2022.934003. eCollection 2022.
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Stem Cell Therapy for Thyroid Diseases: Progress and Challenges.甲状腺疾病的干细胞治疗:进展与挑战
Curr Ther Res Clin Exp. 2022 Mar 5;96:100665. doi: 10.1016/j.curtheres.2022.100665. eCollection 2022.
5
Lymphocyte infiltration and thyrocyte destruction are driven by stromal and immune cell components in Hashimoto's thyroiditis.淋巴细胞浸润和甲状腺细胞破坏是由桥本甲状腺炎的基质和免疫细胞成分驱动的。
Nat Commun. 2022 Feb 9;13(1):775. doi: 10.1038/s41467-022-28120-2.
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Precision Medicine in Autoimmune Thyroiditis and Hypothyroidism.自身免疫性甲状腺炎和甲状腺功能减退症中的精准医学
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Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis.肌成纤维细胞:皮肤纤维化的功能、形成和分子治疗范围。
Biomolecules. 2021 Jul 23;11(8):1095. doi: 10.3390/biom11081095.
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An update on the pathogenesis of Hashimoto's thyroiditis.桥本甲状腺炎发病机制的研究进展。
J Endocrinol Invest. 2021 May;44(5):883-890. doi: 10.1007/s40618-020-01477-1. Epub 2020 Dec 17.
9
Hashimoto's thyroiditis: An update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation.桥本甲状腺炎:发病机制、诊断方案、治疗策略及潜在恶变更新。
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10
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Front Endocrinol (Lausanne). 2020 Jul 15;11:446. doi: 10.3389/fendo.2020.00446. eCollection 2020.

肌成纤维细胞在超微结构水平上阻碍桥本甲状腺炎的恢复。

MYOFIBROBLASTS HINDER RECOVERY OF HASHIMOTO THYROIDITIS IN THE ULTRASTRUCTURAL LEVEL.

作者信息

Theotokis P, Gkantaras A, Avramidou E, Meditskou S, Manthou M E

机构信息

Aristotle University of Thessaloniki, School of Medicine, Laboratory of Histology and Embryology.

Aristotle University of Thessaloniki, Hippocrateion General Hospital, First Department of Pediatrics, Thessaloniki, Greece.

出版信息

Acta Endocrinol (Buchar). 2023 Oct-Dec;19(4):415-420. doi: 10.4183/aeb.2023.415. Epub 2024 Jun 24.

DOI:10.4183/aeb.2023.415
PMID:38933253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11197825/
Abstract

BACKGROUND

Hashimoto thyroiditis (HT) is an autoimmune disorder associated with hypothyroidism. Lymphocyte infiltration leading to thyroid follicular cell destruction is counteracted by increased collagen production, deposition and scarring. However, only recently a specific subpopulation of modified fibroblasts with contractile properties, namely "myofibroblasts" (MFBs) have been linked to HT.

AIM

Our ultrastructural study aims to delineate the presence and contribution of MFBs to the fibrotic milieu of HT.

MATERIAL AND METHODS

Tissue biopsies were obtained from 5 HT-diagnosed patients and specimens were examined using a Transmission Electron Microscope (TEM).

RESULTS

Histopathological examination indicated extensive microvilli atrophy and atypical vacuolations of the thyroid follicular cells in the HT samples. In addition to interstitial extravasated lymphocytes, capillaries were encircled by MFBs (mean distance from lumen 1.248± 0.43µm) with the characteristic electron-dense α-smooth muscle actin (α-SMA), confirmable in higher magnifications. Myofibroblastic projections were found to have significantly higher representation near the capillary lumen compared to the impaired endothelial lining (P < 0.01).

CONCLUSION

Our TEM findings suggest that the intrusion of endothelia by myofibroblastic projections can be a significant factor towards the malfunction of follicular cells in HT patients and offer a paradigmal understanding of the ultrastructural interactions that may underlie the HT pathology.

摘要

背景

桥本甲状腺炎(HT)是一种与甲状腺功能减退相关的自身免疫性疾病。淋巴细胞浸润导致甲状腺滤泡细胞破坏,而胶原生成、沉积和瘢痕形成增加可对抗这种破坏。然而,直到最近,具有收缩特性的特定修饰成纤维细胞亚群,即“肌成纤维细胞”(MFBs)才与HT相关联。

目的

我们的超微结构研究旨在描绘MFBs在HT纤维化环境中的存在情况及其作用。

材料与方法

从5例确诊为HT的患者身上获取组织活检样本,并使用透射电子显微镜(TEM)对标本进行检查。

结果

组织病理学检查表明,HT样本中的甲状腺滤泡细胞存在广泛的微绒毛萎缩和非典型空泡形成。除了间质中渗出的淋巴细胞外,毛细血管被MFBs环绕(距管腔的平均距离为1.248±0.43µm),这些MFBs具有特征性的电子致密α平滑肌肌动蛋白(α-SMA),在更高放大倍数下可确认。与受损的内皮衬里相比,发现肌成纤维细胞突起在毛细血管腔附近的表现明显更高(P<0.01)。

结论

我们的TEM研究结果表明,肌成纤维细胞突起侵入内皮可能是导致HT患者滤泡细胞功能障碍的一个重要因素,并为可能构成HT病理学基础的超微结构相互作用提供了一个范例性的理解。