Vanessa Almonte

ORCID: 0000-0002-2813-0072
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About
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Research Areas
  • Ubiquitin and proteasome pathways
  • Wnt/β-catenin signaling in development and cancer
  • Atherosclerosis and Cardiovascular Diseases
  • Connective tissue disorders research
  • Lipid metabolism and disorders
  • Angiogenesis and VEGF in Cancer
  • Protease and Inhibitor Mechanisms
  • Trypanosoma species research and implications
  • Adipokines, Inflammation, and Metabolic Diseases
  • Adipose Tissue and Metabolism
  • Immune cells in cancer
  • ATP Synthase and ATPases Research
  • Hormonal Regulation and Hypertension
  • Macrophage Migration Inhibitory Factor
  • Diet, Metabolism, and Disease
  • Lysosomal Storage Disorders Research
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cancer-related gene regulation
  • Fibroblast Growth Factor Research
  • Cerebrovascular and Carotid Artery Diseases
  • Peroxisome Proliferator-Activated Receptors
  • Nitric Oxide and Endothelin Effects
  • Cardiovascular Function and Risk Factors
  • Regulation of Appetite and Obesity
  • Congenital heart defects research

Albert Einstein College of Medicine
2015-2024

CVPath Institute
2017

Abstract Background Infection with Trypanosoma cruzi , the protozoan parasite that causes Chagas disease, results in chronic infection leads to cardiomyopathy increased mortality and morbidity endemic regions. In a companion study, our group found high‐fat diet (HFD) protected mice from T . ‐induced myocardial damage significantly reduced post‐infection during acute infection. Methods present study metabolic syndrome was induced prior T. by feeding high fat diet. Also, were treated...

10.1002/dmrr.2636 article EN Diabetes/Metabolism Research and Reviews 2015-01-23

Background and aimsAllograft inflammatory factor-1 (AIF1) has been characterized as a pro-inflammatory molecule expressed primarily in the monocyte/macrophage (MP) lineage positively associated with various forms of vascular disease, including atherosclerosis. Studies AIF1 atherosclerosis have relied on mouse models which was overexpressed either myeloid or smooth muscle cells, resulting increased atherosclerotic plaque burden. How physiologic expression contributes to MP biology...

10.1016/j.atherosclerosis.2019.07.022 article EN cc-by-nc-nd Atherosclerosis 2019-07-26

Remodeling of the vessel wall and formation vascular networks are dynamic processes that occur during mammalian embryonic development in adulthood. Plaque excessive neointima hallmarks atherosclerosis injury. As our understanding these complex evolves, there is a need to develop new imaging techniques study underlying mechanisms.We used tissue clearing light-sheet microscopy for 3-dimensional (3D) profiling response carotid artery ligation induction mouse models.Adipo-Clear immunolabeling...

10.1161/circresaha.119.315804 article EN Circulation Research 2020-01-09

Canonical Wnt and sphingosine-1-phosphate (S1P) signaling pathways are highly conserved systems that contribute to normal vertebrate development, with key consequences for immune, nervous, cardiovascular system function; despite these functional overlaps, little is known about Wnt/β-catenin-S1P cross-talk. In the vascular system, both Wnt/β-catenin S1P signals affect vessel maturation, stability, barrier function, but information regarding their potential coordination scant. We report an...

10.1126/sciadv.adg9278 article EN cc-by-nc Science Advances 2024-03-13

Objective— Smooth muscle cells (SMCs) contribute to neointima formation after vascular injury. Although β-catenin expression is induced injury, whether its function essential in SMCs for neointimal growth unknown. Moreover, although inhibitors of have been developed, their effects on SMC not tested. We assessed the requirement short-term homeostasis and response arterial injury investigated growth. Approach Results— used an inducible, conditional genetic deletion adult mice. Uninjured...

10.1161/atvbaha.116.308643 article EN Arteriosclerosis Thrombosis and Vascular Biology 2017-03-17

Abstract The allograft inflammatory factor (AIF) gene family consists of two identified paralogs – AIF1 and AIF1-like ( AIF1L ). encoded proteins, AIF1L, are 80% similar in sequence show conserved tertiary structure. While studies human populations suggest links between metabolic diseases such as obesity diabetes, associations with have not been reported. Drawing parallels based on structural similarity, we postulated that might contribute to disorders, studied it using mouse models. Here...

10.1038/s41598-020-60433-4 article EN cc-by Scientific Reports 2020-02-27

Abstract Aims Graft vascular disease (GVD), a clinically important and highly complex occlusive disease, arises from the interplay of multiple cellular molecular pathways. While intimal lesions are composed predominantly smooth-muscle-like cells (SMLCs), origin these stimuli leading to their accumulation in GVD uncertain. Macrophages have recently been identified as both potential drivers hyperplasia precursors that undergo transdifferentiation become SMLCs non-transplant settings....

10.1093/cvr/cvab289 article EN Cardiovascular Research 2021-09-03

Mouse models enable the study of genetic factors affecting complex pathophysiology metabolic disorders. Here, we identify reductions in leptin levels, food intake, and obesity due to high-fat diet, accompanied by increased sensitivity, mice that harbor E2a-Cre transgene within Obrq2, an quantitative trait locus (QTL) includes gene. Interestingly, loss allograft inflammatory factor-1-like (AIF1L) protein these transgenic leads similar yet marked reversal phenotype, with accelerated weight...

10.1016/j.isci.2022.105058 article EN cc-by-nc-nd iScience 2022-09-03

<b>Abstract ID 56626</b> <b>Poster Board 156</b> Vascular remodeling is associated with target organ damage and fatal cardiovascular events. The molecular mechanisms that control vascular are still poorly understood, limiting effective therapeutic approaches. smooth muscle cells (SMCs), in part via activation of the Wnt/β-catenin signaling pathway, contribute importantly to remodeling. β-catenin C-terminal domain required SMCs for artery formation during embryogenesis, but its role adulthood...

10.1124/jpet.122.566260 article EN Journal of Pharmacology and Experimental Therapeutics 2023-05-18

Introduction: Vascular remodeling is associated with target organ damage and fatal cardiovascular events. The molecular mechanisms that control vascular are still poorly understood, limiting effective therapeutic approaches. β-catenin C-terminal domain required in smooth muscle cells (SMCs) for artery formation during embryogenesis, but its role adulthood unknown. Therefore, the objective of this study was to define importance SMCs remodeling. Hypothesis: signaling neointima after injury....

10.1161/atvb.43.suppl_1.367 article EN Arteriosclerosis Thrombosis and Vascular Biology 2023-05-01

Heart and kidney transplants are effective treatments for end-stage organ failure, but their long-term success is limited by graft vascular disease (GVD), the leading cause of solid transplant failure. This process manifests as concentric thickening vessel walls due to neointimal hyperplasia in donor organ, characterized expansion cells, notably smooth muscle-like cells (SMLCs) macrophages (MPs), which accumulate, proliferate, eventually occlude lumen arteries. Our lab recently reported that...

10.1161/atvb.37.suppl_1.458 article EN Arteriosclerosis Thrombosis and Vascular Biology 2017-05-01

Vascular smooth muscle cells (SMCs), in part via activation of the Wnt/β-catenin signaling pathway, contribute importantly to vascular remodeling. While C-terminal domain β-catenin links pathway gene expression, how this and related molecular mechanisms are involved remodeling is unknown. Inhibitors targeting specifically have been developed, but their use obstructive disease not yet justified because gap knowledge. Our group has previously shown that SMCs essential for arterial wall...

10.1096/fasebj.2022.36.s1.r5593 article EN The FASEB Journal 2022-05-01

Introduction: The β-catenin C-terminal domain (CTD) is required for artery formation during embryogenesis, but its role in vascular remodeling adulthood unknown. Inhibitors targeting specifically the CTD of have been developed, their use obstructive disease not yet justified because this gap knowledge. Loss mouse aortic smooth muscle cells (MASMCs) decreases transcript levels sphingosine-1-phosphate receptor 1 (S1PR1). However, no studies evaluated crosstalk between these proteins...

10.1161/atvb.41.suppl_1.p169 article EN Arteriosclerosis Thrombosis and Vascular Biology 2021-09-01
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