Naringenin: A Promising Therapeutic Agent against Organ Fibrosis DOI Creative Commons
Yanfei Du, Jun Ma, Yu Fan

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2021, Volume and Issue: 2021(1)

Published: Jan. 1, 2021

Fibrosis is the final common pathology of most chronic diseases as seen in heart, liver, lung, kidney, and skin contributes to nearly half death developed countries. Fibrosis, or scarring, mainly characterized by transdifferentiation fibroblasts into myofibroblasts excessive accumulation extracellular matrix (ECM) secreted myofibroblasts. Despite immense efforts made field organ fibrosis over past decades considerable understanding occurrence development gained, there still lack an effective treatment for fibrotic diseases. Therefore, identifying a new therapeutic strategy against unmet clinical need. Naringenin, flavonoid that occurs naturally citrus fruits, has been found confer wide range pharmacological effects including antioxidant, anti-inflammatory, anticancer benefits thus potentially exerting preventive curative on numerous In addition, emerging evidence revealed naringenin can prevent pathogenesis vivo vitro via regulation various pathways involved signaling molecules such transforming growth factor-β1/small mother decapentaplegic protein 3 (TGF-β1/Smad3), mitogen-activated kinase (MAPK), phosphatidylinositol 3-kinase/protein B (PI3K/Akt), sirtuin1 (SIRT1), nuclear factor-kappa (NF-κB), reactive oxygen species (ROS). Targeting these profibrotic could become novel approach management disorders. this review, we present comprehensive summary antifibrotic roles their underlying mechanisms action. As food derived compound, may serve promising drug candidate

Language: Английский

Chronic kidney disease DOI
Paola Romagnani, Giuseppe Remuzzi, Richard J. Glassock

et al.

Nature Reviews Disease Primers, Journal Year: 2017, Volume and Issue: 3(1)

Published: Nov. 22, 2017

Language: Английский

Citations

765

Organ and tissue fibrosis: Molecular signals, cellular mechanisms and translational implications DOI
Ralf Weiskirchen, Sabine Weiskirchen, Frank Tacke

et al.

Molecular Aspects of Medicine, Journal Year: 2018, Volume and Issue: 65, P. 2 - 15

Published: June 30, 2018

Language: Английский

Citations

461

Cellular and molecular mechanisms of kidney fibrosis DOI
Sonja Djudjaj, Peter Boor

Molecular Aspects of Medicine, Journal Year: 2018, Volume and Issue: 65, P. 16 - 36

Published: June 22, 2018

Language: Английский

Citations

377

Emerging therapeutic opportunities for integrin inhibitors DOI Open Access
Robert J. Slack, Simon J. F. Macdonald, James A. Roper

et al.

Nature Reviews Drug Discovery, Journal Year: 2021, Volume and Issue: 21(1), P. 60 - 78

Published: Sept. 17, 2021

Language: Английский

Citations

362

Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment DOI
Lin Chen,

Tian Yang,

Dewen Lu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2018, Volume and Issue: 101, P. 670 - 681

Published: March 22, 2018

Language: Английский

Citations

294

Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold DOI Open Access
Roman D. Bülow, Peter Boor

Journal of Histochemistry & Cytochemistry, Journal Year: 2019, Volume and Issue: 67(9), P. 643 - 661

Published: May 22, 2019

Kidney fibrosis is the common histological end-point of progressive, chronic kidney diseases (CKDs) regardless underlying etiology. The hallmark renal fibrosis, similar to all other organs, pathological deposition extracellular matrix (ECM). Renal ECM a complex network collagens, elastin, and several glycoproteins proteoglycans forming basal membranes interstitial space. Several functions beyond providing scaffold organ stability are being increasingly recognized, for example, in inflammation. composition determined by function each compartments kidney, that is, glomeruli, tubulo-interstitium, vessels. dynamic structure undergoing remodeling, particularly during fibrosis. From clinical perspective, proteins directly involved rare indirectly CKD progression could serve as specific non-invasive biomarkers scaffolds regenerative medicine. gold standard currently only means measure biopsy, but new diagnostic approaches appearing. Here, we discuss localization, function, remodeling major components healthy diseased, fibrotic kidneys potential use diagnostics tissue engineering.

Language: Английский

Citations

294

Targeting renal fibrosis: Mechanisms and drug delivery systems DOI

Madalina V. Nastase,

Jinyang Zeng-Brouwers,

Małgorzata Wygrecka

et al.

Advanced Drug Delivery Reviews, Journal Year: 2017, Volume and Issue: 129, P. 295 - 307

Published: Dec. 27, 2017

Language: Английский

Citations

239

The role of PI3K/Akt signaling pathway in chronic kidney disease DOI
Hongshuang Wang,

Lanjun Gao,

Chenchen Zhao

et al.

International Urology and Nephrology, Journal Year: 2024, Volume and Issue: 56(8), P. 2623 - 2633

Published: March 18, 2024

Language: Английский

Citations

20

PDGF in organ fibrosis DOI
Barbara M. Klinkhammer, Jürgen Floege, Peter Boor

et al.

Molecular Aspects of Medicine, Journal Year: 2017, Volume and Issue: 62, P. 44 - 62

Published: Nov. 22, 2017

Language: Английский

Citations

170

Runt-Related Transcription Factor 1 (RUNX1) Promotes TGF-β-Induced Renal Tubular Epithelial-to-Mesenchymal Transition (EMT) and Renal Fibrosis through the PI3K Subunit p110δ DOI Creative Commons

Tong Zhou,

Maocai Luo, Wei Cai

et al.

EBioMedicine, Journal Year: 2018, Volume and Issue: 31, P. 217 - 225

Published: May 1, 2018

Renal fibrosis is widely considered a common mechanism leading to end-stage renal failure. Epithelial-to-mesenchymal transition (EMT) plays important roles in the pathogenesis of fibrosis. Runt-related transcription factor 1(RUNX1) vital role hematopoiesis via Endothelial-to-Hematopoietic Transition (EHT), process that conceptually similar EMT, but its EMT and unclear. Here, we demonstrate RUNX1 overexpressed processes TGF-β-induced partial expression level SMAD3-dependent. Knockdown attenuated both phenotypic changes levels marker genes tubular epithelial cells (RTECs). In addition, overexpression promoted cells. Moreover, by increasing PI3K subunit p110δ, which mediated Akt activation. Specific deletion Runx1 mouse RTECs fibrosis, was induced unilateral ureteral obstruction (UUO) folic acid (FA) treatment. These findings suggest potential target for preventing

Language: Английский

Citations

137