Cellular and Molecular Mechanisms of Chronic Inflammation-Associated Organ Fibrosis

Tsukui, Tohru; Shichino, Shigeyuki; Shimaoka, Takeshi; Ueha, Satoshi; Matsushima, Kouji

doi:10.1007/978-4-431-56068-5_2

Cited by 2 publications

(3 citation statements)

References 119 publications

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“…The increase in pro-fibrotic cytokine expression caused by these immune cells is associated with myofibroblast conversion from tissue-resident fibroblast and bone marrow-derived mesenchymal stem cells (MSC), epithelial-to-mesenchymal transition (EMT), and EndoMT. Myofibroblast deposition subsequently promotes excessive ECM production [ 70 , 71 ]. On the other hand, autoantibodies such as anti-MMP-1, anti-MMP-3, and anti-fibrin bound tPA antibodies have been identified in SSc patients, and TIMPs are elevated in SSc [ 58 , 72 , 73 , 74 , 75 , 76 ], and these factors suppress ECM degradation.…”

Section: α2ap and Immune Abnormalities In Sscmentioning

confidence: 99%

“…This process usually occurs over many months or years and causes organ damage or death. The progression of fibrosis is considered to result from maladaptive repair processes caused by profibrotic factors such as TGF-β, CTGF, AngII, PDGF, IFN-γ, and HMGB1, and the profibrotic factors induce myofibroblast differentiation from tissue-resident fibroblasts and bone marrow-derived mesenchymal stem cells (MSCs), epithelial-to-mesenchymal transition (EMT) and EndoMT [ 55 , 70 , 71 , 109 , 110 , 111 ]. In addition, PGF 2α is elevated in SSc patients and is associated with fibrosis progression independently of TGF-β [ 112 , 113 ].…”

Section: α2ap and Fibrosis In Sscmentioning

confidence: 99%

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α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis

Kanno

Shu

2022

Life

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Systemic sclerosis is a connective tissue disease of unknown origin that is characterized by immune system abnormalities, vascular damage, and extensive fibrosis of the skin and visceral organs. α2-antiplasmin is known to be the main plasmin inhibitor and has various functions such as cell differentiation and cytokine production, as well as the regulation of the maintenance of the immune system, endothelial homeostasis, and extracellular matrix metabolism. The expression of α2-antiplasmin is elevated in dermal fibroblasts from systemic sclerosis patients, and the blockade of α2-antiplasmin suppresses fibrosis progression and vascular dysfunction in systemic sclerosis model mice. α2-antiplasmin may have promise as a potential therapeutic target for systemic sclerosis. This review considers the role of α2-antiplasmin in the progression of systemic sclerosis.

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Section: α2ap and Immune Abnormalities In Sscmentioning

confidence: 99%

Section: α2ap and Fibrosis In Sscmentioning

confidence: 99%

α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis

Kanno

Shu

2022

Life

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“…Bone morphogenetic protein receptor, type IA (BMPR1A) mediates TNF-a-induced EMT in the skin and primary keratinocytes, indicating that smad1/5/8 signaling is also involved in inflammation-induced EMT (50). Although the etiology of fibrosis is complex and tissuespecific, the EMT frequently occurs during the chronic inflammation-induced fibrosis of various tissues (51). The EMT also contributes to the progression and metastasis of cancer cells, and is involved in suppressing cell senescence and in developing resistance to radiotherapy and chemotherapy (52,53).…”

Section: H19 Mediates Inflammation By Controlling the Emt Inflammatiomentioning

confidence: 99%

The Roles of H19 in Regulating Inflammation and Aging

Wang

Suen

et al. 2020

Front. Immunol.

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Accumulating evidence suggests that long non-coding RNA H19 correlates with several aging processes. However, the role of H19 in aging remains unclear. Many studies have elucidated a close connection between H19 and inflammatory genes. Chronic systemic inflammation is an established factor associated with various diseases during aging. Thus, H19 might participate in the development of age-related diseases by interplay with inflammation and therefore provide a protective function against age-related diseases. We investigated the inflammatory gene network of H19 to understand its regulatory mechanisms. H19 usually controls gene expression by acting as a microRNA sponge, or through mir-675, or by leading various protein complexes to genes at the chromosome level. The regulatory gene network has been intensively studied, whereas the biogenesis of H19 remains largely unknown. This literature review found that the epithelialmesenchymal transition (EMT) and an imprinting gene network (IGN) might link H19 with inflammation. Evidence indicates that EMT and IGN are also tightly controlled by environmental stress. We propose that H19 is a stress-induced long non-coding RNA. Because environmental stress is a recognized age-related factor, inflammation and H19 might serve as a therapeutic axis to fight against age-related diseases.

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Cellular and Molecular Mechanisms of Chronic Inflammation-Associated Organ Fibrosis

Cited by 2 publications

References 119 publications

α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis

α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis

The Roles of H19 in Regulating Inflammation and Aging

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