Yuan Jiang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Yuan Jiang has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- Jing Hou
Central Laboratory of Qinghai University Affiliated Hospital, Qinghai University Affiliated Hospital, Xining 810000, China
2 shared publications - Dengliang Huang
Central Laboratory of Qinghai University Affiliated Hospital, Qinghai University Affiliated Hospital, Xining 810000, China
1 shared publication - Jun Jiang
Department of Medical Oncology, Qinghai University Affiliated Hospital, Xining, China
1 shared publication Lei Jiang
1 shared publication- Li Sun
Central Laboratory of Qinghai University Affiliated Hospital, Qinghai University Affiliated Hospital, Xining 810000, China
1 shared publication - Meiyuan Tian
Qinghai University, Xining, Qinghai Province, 810001, China; Central Laboratory, Affiliated Hospital of Qinghai University, Xining, Qinghai Province, 810001, China
1 shared publication
Latest Publications
- Open Access
- 11 February 2026
- Published by Elsevier in Sensors and Actuators Reports
- Vol. 11
A one-pot CRISPR-Cas12a mediated exponential amplification assay for sensitive detection of extracellular vesicle microRNAs in lung cancer diagnosis
- 11 February 2026
- Published by Elsevier in Sensors and Actuators Reports
- Vol. 11
Open AccessA one-pot CRISPR-Cas12a mediated exponential amplification assay for sensitive detection of extracellular vesicle microRNAs in lung cancer diagnosis
- Open Access
Mitochondrial Network Fragmentation Leads to Dysfunction of Macrophages During Echinococcus multilocularis Protoscoleces Infection
Alveolar echinococcosis (AE) is a fatal foodborne parasitic disease caused by the larvae of Echinococcus multilocularis. The disease primarily affects the liver. Previous studies have found that Kupffer cells have an immune protective effect, but in the late stages of AE, they are associated with parasite immune escape. The present study analyzed the effects of Echinococcus multilocularis protoscoleces (PSCs) infection on the mitochondrial morphology and function of macrophages, as well as their phagocytic function and apoptosis. Infection with PSCs has been shown to result in the fragmentation of the macrophage mitochondrial network, the impairment of mitochondrial membrane potential, the elevation of mitochondrial reactive oxygen species, and the reduction in mitochondrial DNA copy number. This cascade of events, consequent to the infection, has been demonstrated to promote the apoptosis of macrophages and impair their phagocytic function. Inhibiting mitochondrial fission during PSCs infection has been shown to mitigate mitochondrial dysfunction, suppress macrophage apoptosis, and enhance macrophage phagocytic function. This discovery provides insights into improving macrophage function during the progression of AE.
Open AccessMitochondrial Network Fragmentation Leads to Dysfunction of Macrophages During Echinococcus multilocularis Protoscoleces Infection
Alveolar echinococcosis (AE) is a fatal foodborne parasitic disease caused by the larvae of Echinococcus multilocularis. The disease primarily affects the liver. Previous studies have found that Kupffer cells have an immune protective effect, but in the late stages of AE, they are associated with parasite immune escape. The present study analyzed the effects of Echinococcus multilocularis protoscoleces (PSCs) infection on the mitochondrial morphology and function of macrophages, as well as their phagocytic function and apoptosis. Infection with PSCs has been shown to result in the fragmentation of the macrophage mitochondrial network, the impairment of mitochondrial membrane potential, the elevation of mitochondrial reactive oxygen species, and the reduction in mitochondrial DNA copy number. This cascade of events, consequent to the infection, has been demonstrated to promote the apoptosis of macrophages and impair their phagocytic function. Inhibiting mitochondrial fission during PSCs infection has been shown to mitigate mitochondrial dysfunction, suppress macrophage apoptosis, and enhance macrophage phagocytic function. This discovery provides insights into improving macrophage function during the progression of AE.