Endothelial to mesenchymal transition in kidney fibrosis DOI
Marleen E Jacobs, Dorottya K. de Vries, Marten A. Engelse

et al.

Nephrology Dialysis Transplantation, Journal Year: 2023, Volume and Issue: 39(5), P. 752 - 760

Published: Nov. 15, 2023

ABSTRACT Fibrotic diseases are characterized by the uncontrolled accumulation of extracellular matrix (ECM) components leading to disruption tissue homeostasis. Myofibroblasts as main ECM-producing cells can originate from various differentiated cell types after injury. Particularly, process endothelial-to-mesenchymal transition (endMT), describing phenotypic shifts endothelial adopt a fully mesenchymal identity, may contribute pool myofibroblasts in fibrosis, while capillary rarefaction and exacerbation hypoxia. In renal disease, incomplete recovery acute kidney injury (AKI) ensuing fibrotic reaction stand out major contributors chronic disease (CKD) development. While focus has largely been on impaired tubular epithelial repair potential fibrosis-driving mechanism, alterations microcirculation post-AKI, particular endMT maladaptive response, could hold equal significance. Dysfunctional interplays among microenvironment instigate endMT. Transforming growth factor beta (TGF-β) signaling, with its downstream activation canonical/Smad-mediated non-canonical pathways, identified primary driver this process. However, non-TGF-β-mediated pathways involving inflammatory agents metabolic intercellular communication within also trigger These harmful, cell–cell interactions signaling offer targets for therapeutic intervention impede decelerate fibrogenesis such AKI–CKD progression. Presently, partial reduction TGF-β using anti-diabetic drugs or statins context. Nevertheless, further investigation is warranted validate underlying mechanisms assess positive effects clinical framework.

Language: Английский

The evolving functions of the vasculature in regulating adipose tissue biology in health and obesity DOI
Ibrahim AlZaim, Laura de Rooij, Bilal N. Sheikh

et al.

Nature Reviews Endocrinology, Journal Year: 2023, Volume and Issue: 19(12), P. 691 - 707

Published: Sept. 25, 2023

Language: Английский

Citations

42
Dysregulated cellular metabolism in atherosclerosis: mediators and therapeutic opportunities DOI

Chad Stroope,

Felix Sebastian Nettersheim, Brian G. Coon

et al.

Nature Metabolism, Journal Year: 2024, Volume and Issue: 6(4), P. 617 - 638

Published: March 26, 2024

Language: Английский

Citations

21
Reconceptualizing Endothelial-to-mesenchymal transition in atherosclerosis: Signaling pathways and prospective targeting strategies DOI Creative Commons

Nanlin You,

Guohao Liu, Mengchen Yu

et al.

Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

The modification of endothelial cells (ECs) biological function under pathogenic conditions leads to the expression mesenchymal stromal (MSCs) markers, defined as endothelial-to-mesenchymal transition (EndMT). Invisible in onset and slow progression, atherosclerosis (AS) is a potential contributor various atherosclerotic cardiovascular diseases (ASCVD). By triggering AS, EndMT, "initiator" induces progression ASCVD such coronary heart disease (CHD) ischemic cerebrovascular (ICD), with serious clinical complications myocardial infarction (MI) stroke. In-depth research pathomechanisms EndMT identification targeted therapeutic strategies hold considerable value for prevention treatment ASCVD-associated delayed EndMT. Although previous studies have progressively unraveled complexity its pathogenicity triggered by alterations vascular microenvironmental factors, systematic descriptions most recent roles strategies, their future directions are scarce.

Language: Английский

Citations

2
Zn-DHM nanozymes regulate metabolic and immune homeostasis for early diabetic wound therapy DOI
Shuo Zhang, Xinyu Zhao, Wei Zhang

et al.

Bioactive Materials, Journal Year: 2025, Volume and Issue: 49, P. 63 - 84

Published: March 6, 2025

Language: Английский

Citations

2
Microenvironmental determinants of endothelial cell heterogeneity DOI

Jesús M. Gómez-Salinero,

David Redmond, Shahin Rafii

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 28, 2025

Language: Английский

Citations

1
GPER1/ACACB are potential target genes associated with intracranial aneurysm and vascular endothelial cell senescence DOI
Lang Zeng, Xuanzhen Lu, Yuzhen Huang

et al.

Neurosurgical Review, Journal Year: 2025, Volume and Issue: 48(1)

Published: March 25, 2025

Language: Английский

Citations

1
Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology DOI Open Access
Aman Singh,

Kriti Bhatt,

Hien C. Nguyen

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(11), P. 6180 - 6180

Published: June 4, 2024

Under different pathophysiological conditions, endothelial cells lose phenotype and gain mesenchymal cell-like via a process known as endothelial-to-mesenchymal transition (EndMT). At the molecular level, expression of cell-specific markers such CD31/platelet-endothelial cell adhesion molecule, von Willebrand factor, vascular-endothelial cadherin α-smooth muscle actin, N-cadherin, vimentin, fibroblast specific protein-1, collagens. EndMT is induced by numerous pathways triggered modulated multiple often redundant mechanisms in context-dependent manner depending on status cell. plays an essential role embryonic development, particularly atrioventricular valve development; however, also implicated pathogenesis several genetically determined acquired diseases, including malignant, cardiovascular, inflammatory, fibrotic disorders. Among cardiovascular aberrant reported atherosclerosis, pulmonary hypertension, valvular disease, fibroelastosis, cardiac fibrosis. Accordingly, understanding behind cause and/or effect to eventually target appears be promising strategy for treating EndMT-associated diseases. However, this approach limited lack precise functional pathways, causes effects, robust animal models human data about Here, we review various

Language: Английский

Citations

5
Targeted anti-angiogenesis therapy for advanced osteosarcoma DOI Creative Commons

Qiao Zhang,

Yuxuan Xia,

Liyuan Wang

et al.

Frontiers in Oncology, Journal Year: 2024, Volume and Issue: 14

Published: Aug. 26, 2024

To date, despite extensive research, the prognosis of advanced osteosarcoma has not improved significantly. Thus, patients experience a reduced survival rate, suggesting that reevaluation current treatment strategies is required. Recently, in addition to routine surgery, chemotherapy and radiotherapy, researchers have explored more effective safer treatments, including targeted therapy, immunotherapy, anti-angiogenesis metabolic targets nanomedicine therapy. The tumorigenesis development closely related angiogenesis. therapy crucial treat osteosarcoma; however, recent clinical trials found it insufficient efficacy. solve this problem, causes failure improve should be investigated. This review focuses on summarizing pathophysiological mechanisms angiogenesis advances osteosarcoma. We also discuss some studies, with aim providing new ideas for patients.

Language: Английский

Citations

4
The influence of endothelial metabolic reprogramming on the tumor microenvironment DOI Creative Commons

Kelby M. Kane,

Deanna N. Edwards, Jin Chen

et al.

Oncogene, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 20, 2024

Abstract Endothelial cells (ECs) that line blood vessels act as gatekeepers and shape the metabolic environment of every organ system. In normal conditions, endothelial are relatively quiescent with organ-specific expression signatures profiles. cancer, ECs metabolically reprogrammed to promote formation new fuel tumor growth metastasis. addition EC’s role on cells, tortuous vasculature contributes an immunosuppressive by limiting T lymphocyte infiltration activity while also promoting recruitment other accessory pro-angiogenic immune cells. These elements aid in metastatic spreading cancer contribute therapeutic resistance. The concept restoring a more stabilized concert immunotherapy is emerging potential approach overcoming barriers treatment. This review summarizes metabolism their regulation nutrient uptake delivery, impact shaping microenvironment anti-tumor immunity. We highlight approaches target harness response. Appreciating integration state levels crosstalk among TME may provide avenues for intervention.

Language: Английский

Citations

4
Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition DOI Creative Commons
Cheng Qian, Guanglu Dong, Chunmei Yang

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Jan. 9, 2025

Endothelial-mesenchymal transition (EndMT) is defined as an important process of cellular differentiation by which endothelial cells (ECs) are prone to lose their characteristics and transform into mesenchymal cells. During EndMT, reduced expression adhesion molecules disrupts intercellular adhesion, triggering cytoskeletal reorganization transition. Numerous studies have proved that EndMT a multifaceted biological event driven primarily cytokines such TGF-β, TNF-α, IL-1β, alongside signaling pathways like WNT, Smad, MEK-ERK, Notch. Nevertheless, the exact roles in complicated diseases not been comprehensively reviewed. In this review, we summarize predominant molecular regulatory mechanisms contribute development well highlight contributions series imperative non-coding RNAs curbing initiation EndMT. Furthermore, discuss significant impact on worsening vasculature-related diseases, including cancer, cardiovascular atherosclerosis, pulmonary vascular diabetes-associated fibrotic conditions, cerebral cavernous malformation, providing implications targeting holds promise therapeutic strategy mitigate disease progression.

Language: Английский

Citations

0