Jiaojiao Fan
Role not yet determined Is this you? Add your title
Also affiliated: Shanghai University (2011); Georgia Institute of Technology (2022–2023); Binzhou Medical University (2020); Chongqing University (2018–2019); Beijing University of Chinese Medicine (2025); Shanghai Jiao Tong University (2017–2018); Nantong University (2024); Kyungpook National University (2024); Yale University (2022); Zhengzhou University (2026); Nanjing Children's Hospital (2021–2023); Nanfang Hospital (2019); Kyungil University (2024); Taegu Science University (2024); Shanghai First People's Hospital (2018); Second Affiliated Hospital of Nanjing Medical University (2021–2024); First Affiliated Hospital of Zhengzhou University (2024–2026); Baoding No.1 Central Hospital (2025); State Key Laboratory of Reproductive Medicine (2023–2025); Zhejiang University of Technology (2025); Southern Medical University (2019); Southeast University (2022–2024); Henan Medical University (2018); Nanjing Medical University (2021–2025); Daegu University (2024)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Jiaojiao Fan's research focuses on mechanisms underlying kidney disease and related metabolic disorders. Fan has investigated the role of specific proteins, such as LONP1, in protecting mitochondrial function and mitigating chronic kidney disease progression. Another area of study involves the impact of anti-anemia drugs, like FG4592, on retarding the transition from acute kidney injury to chronic kidney disease by improving vascular regeneration and antioxidative capabilities. Fan has also examined the potential of hypoxia-inducible factor prolyl hydroxylase inhibitors in treating nonanemic diseases and explored how nicotinamide mononucleotide alleviates aluminum-induced bone loss by inhibiting the TXNIP-NLRP3 inflammasome. Additionally, Fan's work includes investigating novel compounds, such as the 3-phenylglutaric acid derivative (84-B10), for their ability to alleviate cisplatin-induced acute kidney injury by targeting mitochondrial oxidative stress-mediated ferroptosis. Fan's publication record includes 62 works with an h-index of 13 and 610 citations.
Metrics
- h-index: 11
- Publications: 53
- Citations: 459
Selected Publications
-
Engineering SIM-1 and MZ-1 PROTACs for enhanced target degradation in KSHV-infected immortalized endothelial cells (2026)
-
Mitochondrial-targeted SS-31 peptide attenuates radiation-induced cardiomyocyte senescence (2026)
-
Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence (2026)
-
Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation (2026)
-
Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin (2026)
-
Roles of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway in Oncovirus Infection and Virus-Associated Cancers (2025)
-
Infection of human induced pluripotent stem cells by an oncogenic herpesvirus (2025)
-
Identification of RP‐54745, an IL‐1 Inhibitor Displaying Anticancer Activities for KSHV‐Related Primary Effusion Lymphoma (2025)
-
Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity (2024)
-
SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence (2024)
-
Roles of Human Endogenous Retrovirus-K-Encoded Np9 in Human Diseases: A Small Protein with Big Functions (2024)
-
Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response (2024)
-
Development of human endogenous retrovirus type K‐ related treatments for human diseases (2024)
-
Mitochondrial proton leak in cardiac aging (2023)
Collaboration Network
Top Collaborators
- Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response
- Roles of Human Endogenous Retrovirus-K-Encoded Np9 in Human Diseases: A Small Protein with Big Functions
- Development of human endogenous retrovirus type K‐ related treatments for human diseases
- Roles of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway in Oncovirus Infection and Virus-Associated Cancers
- Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity
Showing 5 of 9 shared publications
- Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response
- Development of human endogenous retrovirus type K‐ related treatments for human diseases
- Roles of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway in Oncovirus Infection and Virus-Associated Cancers
- Identification of RP‐54745, an IL‐1 Inhibitor Displaying Anticancer Activities for KSHV‐Related Primary Effusion Lymphoma
- Infection of human induced pluripotent stem cells by an oncogenic herpesvirus
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Infection of human induced pluripotent stem cells by an oncogenic herpesvirus
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence
- Mitochondrial proton leak in cardiac aging
- Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin
- Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence
- Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin
- Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation
- Engineering SIM-1 and MZ-1 PROTACs for enhanced target degradation in KSHV-infected immortalized endothelial cells
- Mitochondrial proton leak in cardiac aging
- Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response
- Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity
- Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin
- Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation
- Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin
- Engineering SIM-1 and MZ-1 PROTACs for enhanced target degradation in KSHV-infected immortalized endothelial cells
- Mitochondrial proton leak in cardiac aging
- Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
Similar Researchers
Based on overlapping research topics