Prof. Adnan Erol’s scholarly work explores the molecular relationships between energy metabolism, oxidative and genotoxic stress, cellular signaling, inflammation, aging, neurodegeneration, and malignant transformation.
The publications below represent a thematic selection from his academic work. Complete and continuously updated publication records are available through Google Scholar, PubMed, ResearchGate, and ORCID.
Recent and Current Work
TNFR2-NIK-cAbl Axis for Neurodegeneration
Preprint · 2023
This work examines how TNFR2 signaling, NIK activation, mitochondrial dysfunction, oxidative stress, and c-Abl activity may interact in the development of neurodegenerative processes.
Genotoxicity-Stimulated and CYLD-Driven Malignant Transformation
Cancer Management and Research · 2022
An examination of the molecular interactions connecting genotoxic stress, CYLD activity, NF-κB signaling, redox regulation, and malignant cellular transformation.
DOI: 10.2147/CMAR.S373557
PMID: 35958947
Importance of Efferocytosis in COVID-19 Mortality
Infection and Drug Resistance · 2022
A mechanistic discussion of defective efferocytosis, immune dysregulation, chronic disease, and their possible contribution to severe and fatal COVID-19.
DOI: 10.2147/IDR.S348639
PMID: 35299855
IKK-Mediated CYLD Phosphorylation and Cellular Redox Activity
Molecular Medicine · 2022
This article explores the relationship between IKK signaling, CYLD phosphorylation, NRF2 regulation, oxidative stress, and cellular homeostasis.
DOI: 10.1186/s10020-022-00439-y
PMID: 35109788
Are the Emerging SARS-CoV-2 Mutations Friend or Foe?
Immunology Letters · 2021
A consideration of the biological and clinical implications of emerging SARS-CoV-2 mutations and their possible effects on virulence, transmission, and treatment response.
DOI: 10.1016/j.imlet.2020.12.014
PMID: 33400966
Role of Oxidized LDL-Induced “Trained Macrophages” in the Pathogenesis of COVID-19 and Benefits of Pioglitazone: A Hypothesis
Diabetes & Metabolic Syndrome: Clinical Research & Reviews · 2020
A hypothesis connecting oxidized LDL, trained macrophage responses, atherosclerosis, metabolic disease, and the severity of COVID-19.
DOI: 10.1016/j.dsx.2020.05.007
PMID: 32470851
Cellular Stress, Signal Transduction, and Cancer
Type 2 Diabetes and Cancer as Redox Diseases?
The Lancet · 2014
A discussion of the shared redox and metabolic mechanisms that may connect type 2 diabetes with malignant transformation.
DOI: 10.1016/S0140-6736(14)61486-0
PMID: 25209482
Death-Associated Proliferation Kinetic in Normal and Transformed Cells
Cell Cycle · 2012
An analysis of the relationship between cellular energy metabolism, pyruvate kinase M2, death-associated protein kinase, proliferation, and transformation.
DOI: 10.4161/cc.19723
PMID: 22433951
Genotoxic Stress-Mediated Cell Cycle Activities for the Decision of Cellular Fate
Cell Cycle · 2011
This work investigates how DNA damage responses and cell-cycle signaling influence the cellular choice between repair, senescence, apoptosis, and malignant transformation.
DOI: 10.4161/cc.10.19.17460
PMID: 21921675
Deciphering the Intricate Regulatory Mechanisms for the Cellular Choice Between Cell Repair, Apoptosis or Senescence in Response to Damaging Signals
Cellular Signalling · 2011
An examination of the signaling networks involving p53, FOXO, c-Myc, TGF-β, and other regulators that determine cellular fate following damaging stress.
DOI: 10.1016/j.cellsig.2010.11.023
PMID: 21144894
Metabolic Syndrome Is a Real Disease and Premalignant State Induced by Oncogenic Stresses to Block Malignant Transformation
Medical Hypotheses · 2010
A hypothesis proposing that metabolic syndrome may represent an adaptive response to oncogenic and oxidative stresses that restrict malignant transformation.
DOI: 10.1016/j.mehy.2010.01.001
PMID: 20097480
Retrograde Regulation Due to Mitochondrial Dysfunction May Be an Important Mechanism for Carcinogenesis
Medical Hypotheses · 2005
An exploration of how mitochondrial dysfunction and retrograde signaling may activate metabolic, stress-related, and nuclear pathways involved in carcinogenesis.
DOI: 10.1016/j.mehy.2005.03.022
Metabolism, Aging, and Neurodegeneration
Are Paradoxical Cell Cycle Activities in Neurons and Glia Related to the Metabolic Theory of Alzheimer’s Disease?
Journal of Alzheimer’s Disease · 2010
A discussion of how insulin resistance, oxidative stress, glial senescence, and abnormal neuronal cell-cycle activity may contribute to Alzheimer’s disease.
DOI: 10.3233/JAD-2010-1211
PMID: 20061632
Unraveling the Molecular Mechanisms Behind the Metabolic Basis of Sporadic Alzheimer’s Disease
Journal of Alzheimer’s Disease · 2009
An investigation of peripheral insulin resistance, altered brain energy metabolism, oxidative stress, and their relationship with amyloid and tau pathology.
DOI: 10.3233/JAD-2009-1047
PMID: 19221404
An Integrated and Unifying Hypothesis for the Metabolic Basis of Sporadic Alzheimer’s Disease
Journal of Alzheimer’s Disease · 2008
A proposed integrated model connecting impaired glucose utilization, insulin resistance, central insulin deficiency, oxidative stress, and sporadic Alzheimer’s disease.
DOI: 10.3233/JAD-2008-13302
PMID: 18430992
The Functions of PPARs in Aging and Longevity
PPAR Research · 2007
A review of the roles of peroxisome proliferator-activated receptors in energy metabolism, oxidative stress, inflammation, aging, and age-associated disease.
DOI: 10.1155/2007/39654
PMID: 18317516
Insulin Resistance Is an Evolutionarily Conserved Physiological Mechanism at the Cellular Level for Protection Against Increased Oxidative Stress
BioEssays · 2007
A hypothesis proposing that insulin resistance may initially function as an evolutionarily conserved cellular response protecting against excessive oxidative stress.
DOI: 10.1002/bies.20618
PMID: 17621670
Muscle-Specific PPARβ/δ Agonism May Provide Synergistic Benefits with Lifestyle Modifications
PPAR Research · 2007
A discussion of how muscle-specific PPARβ/δ activation may enhance mitochondrial capacity, fatty-acid oxidation, physical fitness, and metabolic health.
DOI: 10.1155/2007/30578
PMID: 18274626
Complete Publication Records
For the complete publication record, citation information, full-text availability, and the most recent additions, please visit the academic profiles below.