Angiogenesis and experimental hepatic fibrosis

Lemos, Queli Teixeira; Andrade, Zilton A.

doi:10.1590/s0074-02762010000500002

Cited by 14 publications

(13 citation statements)

References 18 publications

(17 reference statements)

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“…With the aid of DEI, we first re-confirm previous pathological findings such as the increase in angiogenesis over time during fibrogenesis [3], [19]. Furthermore, during the regression phase of cirrhosis the quantity of blood vessels does in fact decrease but fails to completely return to normalcy [20], [21].…”

Section: Discussionsupporting

confidence: 75%

A New Conversation between Radiology and Pathology-Identifying Microvascular Architecture in Stages of Cirrhosis via Diffraction Enhanced Imaging In Vitro

Chen

Bihi

et al. 2014

PLoS ONE

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Background/AimDiffraction enhanced imaging (DEI) is a synchrotron radiation X-ray phase-contrast imaging technique that can better reveal the microstructure of biological soft tissues than conventional X-rays. The aim of this study is to investigate the angio-architectural changes of the liver during fibrosis, cirrhosis and its subsequent regression by applying synchrotron radiation based DEI.MethodsDEI experiments were performed at the 4W1A station of Beijing Synchrotron Radiation Facility. Twenty-four Sprague-Dawley rats were induced with liver fibrosis by carbon tetrachloride (CCl4) for up to 10 weeks, after which spontaneous regression started and continued until week 30. Quantitative analysis of the DEI images yielded the mean vascular density and intercapillary distance, which was then re-confirmed by immunohistochemical analysis of CD34.ResultsBased on the DEI results, the mean vascular density was 1.4-fold higher in fibrotic rats (at week 6) and 2-fold higher in cirrhotic rats (at week 10) compared with the control (p<0.05). Accordingly, the intercapillary distance decreased to 563.89±243.35 µm in fibrotic rats and 392.90±92.68 µm in cirrhotic rats compared with 673.85±214.16µm in the control (p<0.05). During fibrosis regression at week 30, vascular density was 0.7-fold lower and intercapillary distance increased to 548.60±210.94 µm as compared with cirrhotic rats (p<0.05).In parallel to the DEI results, immunohistochemical analysis of CD34 showed similar changes.ConclusionSynchrotron-based DEI can conduct radiological as well as pathological analysis. Our results are consistent with previous reports indicating that angiogenesis is directly proportional to fibrosis progression. Furthermore, by clarifying the vascular characteristics of liver diseases, DEI reveals that cirrhosis cannot fully reverse during fibrosis regression.

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Section: Discussionsupporting

confidence: 75%

A New Conversation between Radiology and Pathology-Identifying Microvascular Architecture in Stages of Cirrhosis via Diffraction Enhanced Imaging In Vitro

Chen

Bihi

et al. 2014

PLoS ONE

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“…More specifically, the small molecule inhibitor, LY2109761, natural compound derivatives (halofuginone and quercetin), and siRNA have been used to target various components of the TGF-β pathway to mitigate inflammation, matrix deposition, and fibrosis. Integrin receptors also play an important role in cell–matrix interactions, and inhibition of α5β6 integrin with a specific antibody prevented fibrosis in a mouse model (Flechsig et al 2012; Horton et al 2013c; Lemos and Andrade 2010; Li et al 2006; Xavier et al 2004). Apart from TGF-β and its downstream effectors, targeting other signaling pathways has also yielded promising results in preclinical models.…”

Section: Methodsmentioning

confidence: 99%

Radiation-induced fibrosis: mechanisms and implications for therapy

Straub

New

Hamilton

et al. 2015

J Cancer Res Clin Oncol

415

357

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Purpose Radiation-induced fibrosis (RIF) is a long-term side effect of external beam radiation therapy for the treatment of cancer. It results in a multitude of symptoms that significantly impact quality of life. Understanding the mechanisms of RIF-induced changes is essential to developing effective strategies to prevent long-term disability and discomfort following radiation therapy. In this review, we describe the current understanding of the etiology, clinical presentation, pathogenesis, treatment, and directions of future therapy for this condition. Methods A literature review of publications describing mechanisms or treatments of RIF was performed. Specific databases utilized included PubMed and clinicaltrials.gov, using keywords “Radiation-Induced Fibrosis,” “Radiotherapy Complications,” “Fibrosis Therapy,” and other closely related terms. Results RIF is the result of a misguided wound healing response. In addition to causing direct DNA damage, ionizing radiation generates reactive oxygen and nitrogen species that lead to localized inflammation. This inflammatory process ultimately evolves into a fibrotic one characterized by increased collagen deposition, poor vascularity, and scarring. Tumor growth factor beta serves as the primary mediator in this response along with a host of other cytokines and growth factors. Current therapies have largely been directed toward these molecular targets and their associated signaling pathways. Conclusion Although RIF is widely prevalent among patients undergoing radiation therapy and significantly impacts quality of life, there is still much to learn about its pathogenesis and mechanisms. Current treatments have stemmed from this understanding, and it is anticipated that further elucidation will be essential for the development of more effective therapies.

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“…[126][127][128][129] These processes appear to act in concert and may be co-dependently linked through chronic inflammation. 130,131 HCC relies heavily on angiogenesis to meet its metabolic needs for tumour growth and metastasis [132][133][134] and local tissue hypoxia may act as a trigger for synthesis of angiogenic factors through a HIF-1a-dependent pathway. Increased intrahepatic vascular resistance associated with cirrhosis may also stimulate compensatory vascular remodeling which further exacerbates the condition.…”

Section: Activatedmentioning

confidence: 99%

The role of chemokines in acute and chronic hepatitis C infection

2013

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Hepatitis C imposes a significant burden on global healthcare. Chronic infection is associated with progressive inflammation of the liver which typically manifests in cirrhosis, organ failure and cancer. By virtue of elaborate evasion strategies, hepatitis C virus (HCV) succeeds as a persistent human virus. It has an extraordinary capacity to subvert the immune response enabling it to establish chronic infections and associated liver disease. Chemokines are low molecular weight chemotactic peptides that mediate the recruitment of inflammatory cells into tissues and back into the lymphatics and peripheral blood. Thus, they are central to the temporal and spatial distribution of effector and regulatory immune cells. The interactions between chemokines and their cognate receptors help shape the immune response and therefore, have a major influence on the outcome of infection. However, chemokines represent a target for modulation by viruses including the HCV. HCV is known to modulate chemokine expression in vitro and may therefore enable its survival by subverting the immune response in vivo through altered leukocyte chemotaxis resulting in impaired viral clearance and the establishment of chronic low-grade inflammation. In this review, the roles of chemokines in acute and chronic HCV infection are described with a particular emphasis placed on chemokine modulation as a means of immune subversion. We provide an in depth discussion of the part played by chemokines in mediating hepatic fibrosis while addressing the potential applications for these chemoattractants in prognostic medicine.

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Angiogenesis and experimental hepatic fibrosis

Cited by 14 publications

References 18 publications

A New Conversation between Radiology and Pathology-Identifying Microvascular Architecture in Stages of Cirrhosis via Diffraction Enhanced Imaging In Vitro

A New Conversation between Radiology and Pathology-Identifying Microvascular Architecture in Stages of Cirrhosis via Diffraction Enhanced Imaging In Vitro

Radiation-induced fibrosis: mechanisms and implications for therapy

The role of chemokines in acute and chronic hepatitis C infection

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