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

и другие.

Nephrology Dialysis Transplantation, Год журнала: 2023, Номер 39(5), С. 752 - 760

Опубликована: Ноя. 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.

Язык: Английский

Targeted anti-angiogenesis therapy for advanced osteosarcoma DOI Creative Commons

Qiao Zhang,

Yuxuan Xia,

Liyuan Wang

и другие.

Frontiers in Oncology, Год журнала: 2024, Номер 14

Опубликована: Авг. 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.

Язык: Английский

Процитировано

4
Endothelial Cpt1a Inhibits Neonatal Hyperoxia‐Induced Pulmonary Vascular Remodeling by Repressing Endothelial‐Mesenchymal Transition DOI Creative Commons
Xiaoyun Li, Katy Hegarty, Fanjie Lin

и другие.

Advanced Science, Год журнала: 2025, Номер unknown

Опубликована: Янв. 12, 2025

Abstract Pulmonary hypertension (PH) increases the mortality of preterm infants with bronchopulmonary dysplasia (BPD). There are no curative therapies for this disease. Lung endothelial carnitine palmitoyltransferase 1a (Cpt1a), rate‐limiting enzyme shuttle system, is reduced in a rodent model BPD. It unknown whether Cpt1a reduction causes pulmonary vascular (PV) remodeling. The latter can be result endothelial‐mesenchymal transition (EndoMT). Here, cell (EC)‐specific KO and WT mice (<12 h old) exposed to hyperoxia (70% O 2 ) 14 days allow them recover normoxia until postnatal day 28. Hyperoxia PH, which aggravated EC‐specific mice. Upregulating expression inhibits hyperoxia‐induced PV lung EndoMT, detected by immunofluorescence, scRNA‐sequencing, EC lineage tracing, further increased Blocking EndoMT Male under same high oxygen conditions develop higher degree PH than females, associated expression. Conclusively, neonatal decreasing upregulating EndoMT. This provides valuable strategy developing targeted levels or inhibiting treat BPD‐associated PH.

Язык: Английский

Процитировано

0
Intranuclear TCA and mitochondrial overload: the nascent sprout of tumors metabolism DOI

Weixi Yuan,

Guozhong Lu, Yin Zhao

и другие.

Cancer Letters, Год журнала: 2025, Номер unknown, С. 217527 - 217527

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0
Isoforskolin, adenylate cyclase agonist, inhibits endothelial-to-mesenchymal transition in atherosclerosis DOI

Yiming Ma,

Yunke Shi,

Jinping Lun

и другие.

Phytomedicine, Год журнала: 2025, Номер 139, С. 156520 - 156520

Опубликована: Фев. 16, 2025

Язык: Английский

Процитировано

0
Secretomes From Non‐Small Cell Lung Cancer Cells Induce Endothelial Plasticity Through a Partial Endothelial‐to‐Mesenchymal Transition DOI Creative Commons

Clara Bourreau,

E. Navarro,

Marine Cotinat

и другие.

Cancer Medicine, Год журнала: 2025, Номер 14(5)

Опубликована: Март 1, 2025

The tumor microenvironment (TME) of non-small cell lung cancer (NSCLC) is highly heterogeneous and involved in tumorigenesis resistance to therapy. Among the cells TME, endothelial are associated with latter processes through endothelial-to-mesenchymal transition (EndMT). During EndMT, (ECs) progressively lose their phenotype favor a mesenchymal phenotype, which favors production cancer-associated fibroblasts (CAFs). Our study aimed investigate consequences exposure different secretomes on EC plasticity. Conditioned media (CM) were prepared from lines A549, H1755, H23, H1437, H1975. Proliferation migration ECs treated these CMs assessed by Cyquant Incucyte technologies, respectively. angiogenic capacity was following tubulogenesis Matrigel. Phenotypic changes detected flow cytometry. Morphological analysis actin fibers performed immunohistochemistry, while proteomic mass spectrometry used identify protein content secretomes. A change found when human umbilical vein (HUVECs) CMs. This phenotypic morphological change, an increase both stress fiber expression spontaneous migration. Furthermore, markers (α-SMA CD44) confirmed changes. However, did not modify rate double-labeled (vWF+/α-SMA+ or CD31+/CD44+). Proteomic identified potential targets EndMT therapeutic relevance. Taken together, data suggest that can induce partial EndMT.

Язык: Английский

Процитировано

0
Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis DOI Creative Commons
Francisco Santos, Hashum Sum, Dandan Yan

и другие.

Cells, Год журнала: 2025, Номер 14(5), С. 378 - 378

Опубликована: Март 5, 2025

Endothelial dysfunction is the main initiating factor in atherosclerosis. Through mechanotransduction, shear stress regulates endothelial cell function both homeostatic and diseased states. Accumulating evidence reveals that epigenetic changes play critical roles etiology of cardiovascular diseases, including The metabolic regulation epigenetics has emerged as an important control gene expression states, but to best our knowledge, this connection remains largely unexplored In review, we (1) summarize how (or flow) (dys)function; (2) explore alterations occur endothelium response disturbed flow; (3) review metabolism under different conditions; (4) suggest mechanisms which may link altered epigenome by modulations metabolite availability. We believe plays role reprogramming could pave way for novel metabolism-based therapeutic strategies.

Язык: Английский

Процитировано

0
SNAI2, a potential crossing point between cancer and cardiovascular disease DOI Open Access
Zi-Hao Liu, Yingzi Wang, Lei Li

и другие.

The FASEB Journal, Год журнала: 2025, Номер 39(5)

Опубликована: Март 9, 2025

Cancer and cardiovascular disease remain the leading causes of morbidity mortality worldwide, two separate entities share several similarities possible interactions. Patients with cancer may have underlying disease, which is often exacerbated by stress tumor growth or treatment. At same time, cardiotoxicity induced anti-cancer therapies malignant process itself can lead to new diseases. Efforts been made find a rational explanation for this phenomenon. As classical tumor-promoting factor, we notice that SNAI2 simultaneously plays an important pathogenic role in Moreover, there are striking parallels mechanisms CVD, such as shared risk factors (e.g., smoking diabetes), cellular phenotypic switching, metabolic remodeling, all mediated SNAI2. This review aims summarize SNAI2's core linking well explore therapeutic approaches targeting also seeks provide insights into common both CVD.

Язык: Английский

Процитировано

0
Activity-based trapping for multiplex imaging illuminates the hidden role of endogenous formaldehyde in proinflammatory signaling DOI
Yuan Pan,

Xingguang Liang,

Tianruo Shen

и другие.

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Emergence of More Potent PPD-Qs beyond 6PPD-Q in Human Blood and Cerebrospinal Fluid DOI
Mingming Han, Kaihui Xia, Yuan Xue

и другие.

Environmental Science & Technology Letters, Год журнала: 2025, Номер unknown

Опубликована: Апрель 8, 2025

Язык: Английский

Процитировано

0
Acetyl-CoA synthetase 2 alleviates brain injury following cardiac arrest by promoting autophagy in brain microvascular endothelial cells DOI Creative Commons
Wenbin Zhang, Xin Yu, Lin Yao

и другие.

Cellular and Molecular Life Sciences, Год журнала: 2025, Номер 82(1)

Опубликована: Апрель 17, 2025

Brain injury is a common sequela following cardiac arrest (CA), with up to 70% of hospitalized patients dying from it. microvascular endothelial cells (BMVECs) play crucial role in post-cardiac brain (PCABI). However, the effects and mechanisms targeting BMVEC energy metabolism mitigate remain unclear. We established mouse model by injecting potassium chloride into right internal jugular vein. Mass spectrometry detected targeted changes short-chain fatty acids metabolites CA/CPR group compared sham group. Mice overexpressed ACSS2 BMVECs were created using an AAV-BR1 vector, knockout mice generated CRE-LOXP system. The oxygen glucose deprivation/re-oxygenation (OGD/R) was investigate vitro. Metabolomics analysis revealed disrupted cerebral post-CA/CPR, decreased acetyl-CoA amino acids. Overexpression increased levels improved neurological function. Vascular cell-specific exhibited reduced aortic sprouting dysfunction influenced autophagy interacting transcription factor EB (TFEB) modulating AMP-activated protein kinase α (AMPKα) pathway. Our study shows that modulates biological functions promoting autophagy. Enhancing via may target PCABI treatment development.

Язык: Английский

Процитировано

0