Eric Cho
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Eric Cho has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
- Hirohito Ichii
Department of Surgery, University of California Irvine, Orange, CA 92868, USA
3 shared publications - Michael Alexander
Department of Surgery, University of California Irvine, Orange, CA 92868, USA
3 shared publications - Eiger Gliozheni
Department of Surgery, University of California Irvine, Orange, CA 92868, USA
2 shared publications - Antoney Ferrey
Department of Medicine, University of California Irvine, Irvine, CA 92697, USA
1 shared publication - Brandon Shams
Department of Surgery, University of California Irvine, Orange, CA 92868, USA
1 shared publication - Dane Olbrich
Department of Surgery, University of California Irvine, Orange, CA 92868, USA
1 shared publication
Latest Publications
- Open Access
- 29 July 2025
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 26 (15) , 7316
Food-Derived Phytochemicals: Multicultural Approaches to Oxidative Stress and Immune Response
This review will focus on how ethnic consumption of foods such as shiitake, ginseng, turmeric, black seeds, berries, rosemary, moringa and holy basil can help act as antioxidants and immune modulators in fighting many diseases. We will investigate how these foods act on pathways like Nrf2/Keap1 to increase endogenous antioxidant capacity and help in reducing ROS production, based on publications found in PubMed between 1994 and 2024. In addition, we will show how these plants can cause immune system shifts by changing the makeup of the ratio of Th1/Th2 cells, reduce inflammation, and have antiangiogenic effects on cancer. This review will also show how plants can alter the gut microbiota and lead to a further decrease in oxidative stress. Overall, it will show how plants and their metabolites can potentially create a path forward for creating novel therapeutic approaches and help lead to an improved redox balance, support immune function, and enhance long-term health outcomes.
- 29 July 2025
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 26 (15) , 7316
Open AccessFood-Derived Phytochemicals: Multicultural Approaches to Oxidative Stress and Immune Response
This review will focus on how ethnic consumption of foods such as shiitake, ginseng, turmeric, black seeds, berries, rosemary, moringa and holy basil can help act as antioxidants and immune modulators in fighting many diseases. We will investigate how these foods act on pathways like Nrf2/Keap1 to increase endogenous antioxidant capacity and help in reducing ROS production, based on publications found in PubMed between 1994 and 2024. In addition, we will show how these plants can cause immune system shifts by changing the makeup of the ratio of Th1/Th2 cells, reduce inflammation, and have antiangiogenic effects on cancer. This review will also show how plants can alter the gut microbiota and lead to a further decrease in oxidative stress. Overall, it will show how plants and their metabolites can potentially create a path forward for creating novel therapeutic approaches and help lead to an improved redox balance, support immune function, and enhance long-term health outcomes.
- Top Cited PapersOpen Access
- 28 June 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (13) , 7105
Pathology of Diabetes-Induced Immune Dysfunction
Diabetes is associated with numerous comorbidities, one of which is increased vulnerability to infections. This review will focus on how diabetes mellitus (DM) affects the immune system and its various components, leading to the impaired proliferation of immune cells and the induction of senescence. We will explore how the pathology of diabetes-induced immune dysfunction may have similarities to the pathways of “inflammaging”, a persistent low-grade inflammation common in the elderly. Inflammaging may increase the likelihood of conditions such as rheumatoid arthritis (RA) and periodontitis at a younger age. Diabetes affects bone marrow composition and cellular senescence, and in combination with advanced age also affects lymphopoiesis by increasing myeloid differentiation and reducing lymphoid differentiation. Consequently, this leads to a reduced immune system response in both the innate and adaptive phases, resulting in higher infection rates, reduced vaccine response, and increased immune cells’ senescence in diabetics. We will also explore how some diabetes drugs induce immune senescence despite their benefits on glycemic control.
- 28 June 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (13) , 7105
Top Cited PapersOpen AccessPathology of Diabetes-Induced Immune Dysfunction
Diabetes is associated with numerous comorbidities, one of which is increased vulnerability to infections. This review will focus on how diabetes mellitus (DM) affects the immune system and its various components, leading to the impaired proliferation of immune cells and the induction of senescence. We will explore how the pathology of diabetes-induced immune dysfunction may have similarities to the pathways of “inflammaging”, a persistent low-grade inflammation common in the elderly. Inflammaging may increase the likelihood of conditions such as rheumatoid arthritis (RA) and periodontitis at a younger age. Diabetes affects bone marrow composition and cellular senescence, and in combination with advanced age also affects lymphopoiesis by increasing myeloid differentiation and reducing lymphoid differentiation. Consequently, this leads to a reduced immune system response in both the innate and adaptive phases, resulting in higher infection rates, reduced vaccine response, and increased immune cells’ senescence in diabetics. We will also explore how some diabetes drugs induce immune senescence despite their benefits on glycemic control.
- Open Access
- 9 January 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (2) , 821
Nrf2 Pathway and Oxidative Stress as a Common Target for Treatment of Diabetes and Its Comorbidities
Diabetes is a chronic disease that induces many comorbidities, including cardiovascular disease, nephropathy, and liver damage. Many mechanisms have been suggested as to how diabetes leads to these comorbidities, of which increased oxidative stress in diabetic patients has been strongly implicated. Limited knowledge of antioxidative antidiabetic drugs and substances that can address diabetic comorbidities through the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway calls for detailed investigation. This review will describe how diabetes increases oxidative stress, the general impact of that oxidative stress, and how oxidative stress primarily contributes to diabetic comorbidities. It will also address how treatments for diabetes, especially focusing on their effects on the Nrf2 antioxidative pathway, have been shown to similarly affect the Nrf2 pathway of the heart, kidney, and liver systems. This review demonstrates that the Nrf2 pathway is a common pathogenic component of diabetes and its associated comorbidities, potentially identifying this pathway as a target to guide future treatments.
- 9 January 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (2) , 821
Open AccessNrf2 Pathway and Oxidative Stress as a Common Target for Treatment of Diabetes and Its Comorbidities
Diabetes is a chronic disease that induces many comorbidities, including cardiovascular disease, nephropathy, and liver damage. Many mechanisms have been suggested as to how diabetes leads to these comorbidities, of which increased oxidative stress in diabetic patients has been strongly implicated. Limited knowledge of antioxidative antidiabetic drugs and substances that can address diabetic comorbidities through the nuclear factor erythroid 2–related factor 2 (Nrf2) pathway calls for detailed investigation. This review will describe how diabetes increases oxidative stress, the general impact of that oxidative stress, and how oxidative stress primarily contributes to diabetic comorbidities. It will also address how treatments for diabetes, especially focusing on their effects on the Nrf2 antioxidative pathway, have been shown to similarly affect the Nrf2 pathway of the heart, kidney, and liver systems. This review demonstrates that the Nrf2 pathway is a common pathogenic component of diabetes and its associated comorbidities, potentially identifying this pathway as a target to guide future treatments.