Osteopontin in Cardiovascular Diseases DOI Creative Commons

Kohsuke Shirakawa,

Motoaki Sano

Biomolecules, Journal Year: 2021, Volume and Issue: 11(7), P. 1047 - 1047

Published: July 16, 2021

Unprecedented advances in secondary prevention have greatly improved the prognosis of cardiovascular diseases (CVDs); however, CVDs remain a leading cause death globally. These findings suggest need to reconsider risk and optimal medical therapy. Numerous studies shown that inflammation, pro-thrombotic factors, gene mutations are focused not only on residual but also as next therapeutic target for CVDs. Furthermore, recent clinical trials, such Canakinumab Anti-inflammatory Thrombosis Outcomes Study trial, showed possibility anti-inflammatory therapy patients with Osteopontin (OPN) is matricellular protein mediates diverse biological functions involved number pathological states OPN has two-faced phenotype dependent state. Acute increases protective roles, including wound healing, neovascularization, amelioration vascular calcification. By contrast, chronic predict poor major adverse event independent conventional factors. Thus, can be clinically available. In this review, we discuss role development its potential target.

Language: Английский

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure DOI Open Access
Anis Hanna, Nikolaos G. Frangogiannis

Cardiovascular Drugs and Therapy, Journal Year: 2020, Volume and Issue: 34(6), P. 849 - 863

Published: Sept. 9, 2020

Language: Английский

Citations

301
Diffuse myocardial fibrosis: mechanisms, diagnosis and therapeutic approaches DOI
Begoña López, Susana Ravassa, María U. Moreno

et al.

Nature Reviews Cardiology, Journal Year: 2021, Volume and Issue: 18(7), P. 479 - 498

Published: Feb. 10, 2021

Language: Английский

Citations

229
Regulation of Collagen I and Collagen III in Tissue Injury and Regeneration DOI

Drishtant Singh,

Vikrant Rai, Devendra K. Agrawal

et al.

Cardiology and Cardiovascular Medicine, Journal Year: 2023, Volume and Issue: 07(01)

Published: Jan. 1, 2023

The structure of connective tissues including cartilage, tendons, and ligaments as well many organs, like the skin, heart, liver, kidney, lungs, blood vessels, bones, depend on collagen. bulk network structural proteins that make up extracellular matrix heart is composed collagen type I III, which provide support for muscle cells are crucial cardiac function. prognosis progression a disease or diseased state may be significantly impacted by upregulation downregulation types, particularly Col III. For example, increasing protein levels impose myocardial stiffness, impairing diastolic systolic function myocardium. Collagen stiff fibrillar gives tensile strength, whereas III produces an elastic stores kinetic energy rebound. These two have distinct physical properties in nature. Therefore, control potential relevance I/Col ratio biological processes serve foundation this comprehensive review article.

Language: Английский

Citations

180
Immune Cells and Immunotherapy for Cardiac Injury and Repair DOI Open Access
Joel G. Rurik, Haig Aghajanian, Jonathan A. Epstein

et al.

Circulation Research, Journal Year: 2021, Volume and Issue: 128(11), P. 1766 - 1779

Published: May 27, 2021

Cardiac injury remains a major cause of morbidity and mortality worldwide. Despite significant advances, full understanding why the heart fails to fully recover function after acute injury, progressive failure frequently ensues, elusive. No therapeutics, short transplantation, have emerged reliably halt or reverse inexorable progression in majority patients once it has become clinically evident. To date, most pharmacological interventions focused on modifying hemodynamics (reducing afterload, controlling blood pressure volume) cardiac myocyte function. However, important contributions immune system normal response recently as exciting areas investigation. Therapeutic aimed at harnessing power cells hold promise for new treatment avenues disease. Here, we review its contribution fibrosis, potential therapies affect repair.

Language: Английский

Citations

179
Role of PI3K/Akt signaling pathway in cardiac fibrosis DOI

Wu-Ming Qin,

Linghui Cao,

Isaac Yaw Massey

et al.

Molecular and Cellular Biochemistry, Journal Year: 2021, Volume and Issue: 476(11), P. 4045 - 4059

Published: July 10, 2021

Language: Английский

Citations

168
Type V Collagen in Scar Tissue Regulates the Size of Scar after Heart Injury DOI Creative Commons
Tomohiro Yokota, Jackie L. McCourt, Feiyang Ma

et al.

Cell, Journal Year: 2020, Volume and Issue: 182(3), P. 545 - 562.e23

Published: July 3, 2020

Language: Английский

Citations

157
Hif-1a suppresses ROS-induced proliferation of cardiac fibroblasts following myocardial infarction DOI Creative Commons
Vaibhao Janbandhu, Vikram J. Tallapragada, Ralph Patrick

et al.

Cell stem cell, Journal Year: 2021, Volume and Issue: 29(2), P. 281 - 297.e12

Published: Nov. 10, 2021

Language: Английский

Citations

152
The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress DOI Open Access
Kazuaki Maruyama, Kyoko Imanaka‐Yoshida

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(5), P. 2617 - 2617

Published: Feb. 27, 2022

Fibrosis is defined as the excessive deposition of extracellular matrix (ECM) proteins in interstitium. It an essential pathological response to chronic inflammation. ECM protein initially protective and critical for wound healing tissue regeneration. However, cardiac remodeling continuous damage with subsequent results a distorted organ architecture significantly impacts function. In this review, we summarized discussed histologic features fibrosis signaling factors that control it. We evaluated origin characteristic markers fibroblasts. also lymphatic vessels, which have become more important recent years improve fibrosis.

Language: Английский

Citations

119
Versican Promotes Cardiomyocyte Proliferation and Cardiac Repair DOI Open Access
Jie Feng, Yandong Li, Yan Li

et al.

Circulation, Journal Year: 2023, Volume and Issue: 149(13), P. 1004 - 1015

Published: Oct. 27, 2023

BACKGROUND: The adult mammalian heart is incapable of regeneration, whereas a transient regenerative capacity maintained in the neonatal heart, primarily through proliferation preexisting cardiomyocytes. Neonatal regeneration after myocardial injury accompanied by an expansion cardiac fibroblasts and compositional changes extracellular matrix. Whether how these influence cardiomyocyte remains to be investigated. METHODS: We used apical resection infarction surgical models mice investigate matrix components involved injury. Single-cell RNA sequencing liquid chromatography–mass spectrometry analyses were for versican identification. Cardiac fibroblast–specific Vcan deletion was achieved using mouse strains Col1a2-2A-CreER fl/fl . Molecular signaling pathways related effects assessed Western blot, immunostaining, quantitative reverse transcription polymerase chain reaction. fibrosis function evaluated Masson trichrome staining echocardiography, respectively. RESULTS: Versican, fibroblast–derived component, upregulated promoted proliferation. Conditional knockout decreased impaired regeneration. In mice, intramyocardial injection enhanced proliferation, reduced fibrosis, improved function. Furthermore, augmented human induced pluripotent stem cell–derived Mechanistically, activated integrin β1 downstream molecules, including ERK1/2 Akt, thereby promoting repair. CONCLUSIONS: Our study identifies as pro-proliferative proteoglycan clarifies role These findings highlight its potential therapeutic factor ischemic diseases.

Language: Английский

Citations

48
Generation of human vascularized and chambered cardiac organoids for cardiac disease modelling and drug evaluation DOI Creative Commons

Jingsi Yang,

Wei Lei,

Yang Xiao

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(8)

Published: March 7, 2024

Abstract Human induced pluripotent stem cell (hiPSC)‐derived cardiac organoids (COs) have shown great potential in modelling human heart development and cardiovascular diseases, a leading cause of global death. However, several limitations such as low reproducibility, limited vascularization difficulty formation chamber were yet to be overcome. We established new method for robust generation COs, via combination methodologies hiPSC‐derived vascular spheres directly differentiated cardiomyocytes from hiPSCs, investigated the application COs injury drug evaluation. The we built displayed vascularized chamber‐like structure, hence named vaschamcardioids (vcCOs). These vcCOs exhibited approximately 90% spontaneous beating ratio. Single‐cell transcriptomics identified total six types vcCOs, including cardiomyocytes, precursor cells, endothelial fibroblasts, etc. successfully recaptured processes fibrosis vivo on showed that FDA‐approved medication captopril significantly attenuated injury‐induced functional disorders. In addition, an obvious toxicity reaction doxorubicin dose‐dependent manner. developed three‐step complex our data suggested might become useful model understanding pathophysiological mechanisms developing intervention strategies screening drugs.

Language: Английский

Citations

18