Skylar D. King

ORCID: 0000-0002-4150-7807
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About
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Research Areas
  • Mitochondrial Function and Pathology
  • Genetics, Aging, and Longevity in Model Organisms
  • Metalloenzymes and iron-sulfur proteins
  • RNA modifications and cancer
  • Neonatal Respiratory Health Research
  • Circadian rhythm and melatonin
  • Fatty Acid Research and Health
  • Trace Elements in Health
  • Advanced Glycation End Products research
  • Polymer composites and self-healing
  • Electrospun Nanofibers in Biomedical Applications
  • Adipokines, Inflammation, and Metabolic Diseases
  • Pulmonary Hypertension Research and Treatments
  • Additive Manufacturing and 3D Printing Technologies
  • Liver Disease and Transplantation
  • Cardiovascular and Diving-Related Complications
  • 3D Printing in Biomedical Research
  • Ferroptosis and cancer prognosis
  • Shakespeare, Adaptation, and Literary Criticism
  • Liver Disease Diagnosis and Treatment
  • Connective tissue disorders research
  • Neuroscience of respiration and sleep
  • Epigenetics and DNA Methylation
  • S100 Proteins and Annexins
  • Birth, Development, and Health

University of Missouri
2020-2024

University of Missouri Hospital
2024

University of North Texas
2016-2018

Programmed cell death, which occurs through a conserved core molecular pathway, is important for fundamental developmental and homeostatic processes. The human iron–sulfur binding protein NAF-1/CISD2 binds to Bcl-2 its disruption in cells leads an increase apoptosis. Other members of the CDGSH iron sulfur domain (CISD) family include mitoNEET/CISD1 Miner2/CISD3. In humans, mutations CISD2 result Wolfram syndrome 2, disease patients display juvenile diabetes, neuropsychiatric disorders...

10.1038/s41418-018-0108-5 article EN cc-by Cell Death and Differentiation 2018-04-17

Individuals with type 2 diabetes display metabolic abnormalities, such as hyperglycemia, increased free fatty acids, insulin resistance, and altered ceramide levels, that contribute to vascular dysfunctions compromised oxygen delivery. Caenorhabditis elegans fed a glucose-supplemented diet or metabolism, due hyl-2 mutation, are sensitive deprivation (anoxia). Our experiments showed the combination of these factors further decreased anoxia survival. RNA-sequencing analysis was performed...

10.1534/g3.116.031583 article EN cc-by G3 Genes Genomes Genetics 2016-08-12

Considered a key aging gene, CISD2 , encoding CDGSH iron–sulfur domain‐containing protein 2, plays central role in regulating calcium homeostasis, preventing mitochondrial dysfunction, and the activation of autophagy apoptosis different cells. Here, we show that cardiomyocytes from ‐null mice accumulate high levels iron contain transferrin receptor ferritin. Using proteomics transmission electron microscopy, further lack induces several features process young mice, but other are not induced....

10.1002/1873-3468.14277 article EN FEBS Letters 2022-01-08

Atherosclerosis is a progressive inflammatory disease where macrophage foam cells play central role in the pathogenesis. Surfactant protein A (SPA) lipid-associating involved with regulating function various diseases. However, of SPA atherosclerosis and cell formation has not been investigated.

10.1101/2023.03.23.533959 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-03-24

BACKGROUND: Atherosclerosis is a progressive inflammatory disease in which macrophage foam cells play central role pathogenesis. SPA (surfactant protein A) lipid-associating involved with regulating function various diseases. However, the of atherosclerosis and cell formation has not been investigated. METHODS: expression was assessed healthy atherosclerotic human coronary arteries brachiocephalic wild-type or ApoE-deficient mice fed high-fat diets for 4 weeks. Hypercholesteremic...

10.1161/atvbaha.124.321460 article EN Arteriosclerosis Thrombosis and Vascular Biology 2024-10-03

Reproductive organs and developing tissues have high energy demands that require metabolic functions primarily supported by mitochondria function. The highly conserved CISD/NEET iron-sulfur (Fe-S) protein family regulates iron reactive oxygen homeostasis, both of which are important for mitochondrial Disruption homeostasis typically leads to detrimental effects. In humans, CISD dysfunction is associated with human health issues including Wolfram syndrome 2. Using C . elegans , we previously...

10.1371/journal.pone.0245174 article EN cc-by PLoS ONE 2021-02-05

The objective of this study is to determine the role SPA (surfactant protein A) in vascular smooth muscle cell (SMC) phenotypic modulation and remodeling. Approach Results: PDGF-BB (Platelet-derived growth factor-BB) serum induced expression while downregulating SMC marker gene SMCs. deficiency increased contractile expression. Mechanistically, enhanced myocardin TGF (transforming factor)-β, key regulators for phenotype. In vivo, was medial neointimal SMCs following mechanical injury both...

10.1161/atvbaha.120.314622 article EN Arteriosclerosis Thrombosis and Vascular Biology 2020-12-03

Abstract Metabolic dysfunction-associated steatotic liver disease (MASLD) remains the most common cause of in United States due to increased incidence metabolic dysfunction and obesity. Surfactant protein A (SPA) regulates macrophage function, strongly binds lipids, is implicated renal idiopathic pulmonary fibrosis (IPF). However, role SPA lipid accumulation, inflammation, hepatic that characterize MASLD unknown. deficient (SPA −/− ) age-matched wild-type (WT) control mice were fed a Western...

10.1038/s41598-024-58291-5 article EN cc-by Scientific Reports 2024-03-29

Vascular smooth muscle cell (SMC) transition from a differentiated to dedifferentiated phenotype and subsequent neointima formation/vascular remodeling plays critical role in the development of number vascular diseases such as atherosclerosis, restenosis after angioplasty or bypass, diabetic complications, arteriopathy transplants, asthma cancer. However, mechanisms that regulate SMC modulation formation are not completely understood. We have found Surfactant protein A (SPA), an innate...

10.1161/circ.146.suppl_1.11944 article EN Circulation 2022-11-08
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