Inhibition of α1‐adrenoceptor reduces TGF‐β1‐induced epithelial‐to‐mesenchymal transition and attenuates UUO‐induced renal fibrosis in mice

Ren, Huiwen; Zuo, Shengkai; Hou, Yayan; Shang, Wenlong; Liu, Na; Yin, Zhuming

doi:10.1096/fj.202000737rrr

Cited by 12 publications

(5 citation statements)

References 57 publications

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“… 17 , 18 , 19 , 20 , 21 Increasing evidence supports the idea that decreasing EMT inhibits these pathways to alleviate renal fibrosis and protect renal function. 22 , 23 , 24 , 25 …”

Section: Introductionmentioning

confidence: 99%

Aerobic exercise inhibits renal EMT by promoting irisin expression in SHR

Luo¹,

Luo²,

Xue³

et al. 2023

iScience

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“… 17 , 18 , 19 , 20 , 21 Increasing evidence supports the idea that decreasing EMT inhibits these pathways to alleviate renal fibrosis and protect renal function. 22 , 23 , 24 , 25 …”

Section: Introductionmentioning

confidence: 99%

Aerobic exercise inhibits renal EMT by promoting irisin expression in SHR

Luo¹,

Luo²,

Xue³

et al. 2023

iScience

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“…Sympathetic overactivation facilitates epithelial mesenchymal transition (EMT) of renal epithelial cells and brosis via the α1-adrenoceptor/p38/Smad3 signaling pathway, while α1-adrenoceptor inhibition may attract promising future attention for treating renal brosis [54]. In the current study, tamsulosin noticeably reduced cardiac brosis mediated by ISO administration.…”

Section: Discussionmentioning

confidence: 64%

α1A-Adrenoreceptor blockade attenuates myocardial infarction by modulating the integrin-linked kinase/TGF-β/Smad signaling pathways

Al-Rasheed

Alammari

Alshammari

et al. 2022

Preprint

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Background The role of α1A-adrenoceptor inhibition or its relationship with integrin-linked kinase (ILK) and transforming growth factor-beta (TGF-β)/small mothers against decapentaplegic (Smad) signaling pathways in attenuating myocardial infarction (MI) is unclear. Objectives To investigate whether tamsulosin, an α1A-adrenoceptor blocker, attenuates MI via modulation of an ILK-related TGFβ/Smad pathway. Methods Twenty-four adult male Wistar rats (150−250 g) were randomly divided into four groups: 1) control group, which received a 0.9% NaCl solution orally for 21 days; 2) tamsulosin-treated group, which received tamsulosin (0.8 mg/kg) for 21 days; 3) isoproterenol (ISO)-treated group, which received 0.9% NaCl for 21 days and ISO (150 mg/kg, ip) injected on days 20 and 21 to induce MI; and 4) tamsulosin + ISO group, treated with tamsulosin for 21 days followed by two ISO injections on two consecutive days. The heart/body weight ratios and cardiac and fibrotic biomarker levels were subsequently measured. ILK, TGF-β1, p-Smad2/3, and collagen III protein expression levels were determined using biomolecular methods. Results Tamsulosin significantly attenuated the relative heart-body index (p < 0.5) and creatine kinase (CK)-MB levels (p < 0.01) compared to the ISO control group. While ISO produced superoxide anions and enhanced oxidative damage, tamsulosin treatment significantly prevented this damage via antioxidant defenses, increasing glutathione and superoxide dismutase levels (p < 0.05) and decreasing lipid peroxide oxidation levels (p < 0.01). Data revealed that tamsulosin reduced expression of TGF-β/p-Smad2/3 and enhanced ILK expression. Conclusion Tamsulosin may exert a cardioprotective effect by modulating the ILK-related TGF-β/Smad signaling pathway. Thus, tamsulosin may be a useful therapeutic approach for preventing MI.

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“…It is possible that increased PRL levels, due to either ectopic pituitary grafts, administration of SSRI, or DRD2 insufficiency, could cause or exacerbate pain, which subsequently activates the hypothalamus–pituitary–adrenal (HPA) axis, resulting in increased release of catecholamines, which, in turn, may activate adrenoreceptors in the endometrium. The activation of adrenoreceptors in the endometrium may induce EMT or collective cell migration [ 145 , 146 , 147 , 148 ], leading to the infiltration of endometrial cells in the myometrium and thus adenomyosis.…”

Section: Resultsmentioning

confidence: 99%

Unveiling the Pathogenesis of Adenomyosis through Animal Models

Wang

Benagiano

Liu

et al. 2022

JCM

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Background: Adenomyosis is a common gynecological disorder traditionally viewed as “elusive”. Several excellent review papers have been published fairly recently on its pathogenesis, and several theories have been proposed. However, the falsifiability, explanatory power, and predictivity of these theories are often overlooked. Since adenomyosis can occur spontaneously in rodents and many other species, the animal models may help us unveil the pathogenesis of adenomyosis. This review critically tallies experimentally induced models published so far, with a particular focus on their relevance to epidemiological findings, their possible mechanisms of action, and their explanatory and predictive power. Methods: PubMed was exhaustively searched using the phrase “adenomyosis and animal model”, “adenomyosis and experimental model”, “adenomyosis and mouse”, and “adenomyosis and rat”, and the resultant papers were retrieved, carefully read, and the resultant information distilled. All the retrieved papers were then reviewed in a narrative manner. Results: Among all published animal models of adenomyosis, the mouse model of adenomyosis induced by endometrial–myometrial interface disruption (EMID) seems to satisfy the requirements of falsifiability and has the predictive capability and also Hill’s causality criteria. Other theories only partially satisfy Hill’s criteria of causality. In particular, animal models of adenomyosis induced by hyperestrogenism, hyperprolactinemia, or long-term exposure to progestogens without much epidemiological documentation and adenomyosis is usually not the exclusive uterine pathology consequent to those induction procedures. Regardless, uterine disruption appears to be a necessary but not sufficient condition for causing adenomyosis. Conclusions: EMID is, however, unlikely the sole cause for adenomyosis. Future studies, including animal studies, are warranted to understand how and why in utero and/or prenatal exposure to elevated levels of estrogen or estrogenic compounds increases the risk of developing adenomyosis in adulthood, to elucidate whether prolactin plays any role in its pathogenesis, and to identify sufficient condition(s) that cause adenomyosis.

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Inhibition of α1‐adrenoceptor reduces TGF‐β1‐induced epithelial‐to‐mesenchymal transition and attenuates UUO‐induced renal fibrosis in mice

Cited by 12 publications

References 57 publications

Aerobic exercise inhibits renal EMT by promoting irisin expression in SHR

Aerobic exercise inhibits renal EMT by promoting irisin expression in SHR

α1A-Adrenoreceptor blockade attenuates myocardial infarction by modulating the integrin-linked kinase/TGF-β/Smad signaling pathways

Unveiling the Pathogenesis of Adenomyosis through Animal Models

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