Jiaojiao Fan
Researcher
Also affiliated: Shanghai University (2011); Georgia Institute of Technology (2023); Binzhou Medical University (2020); Shandong University of Aeronautics (2020); Chongqing University (2018–2019); Hunan University (2018); Zhejiang University of Science and Technology (2025); Shanghai Jiao Tong University (2017–2018); Nantong University (2024); Nanjing Children's Hospital (2022–2025); Nanfang Hospital (2019); Creative Commons (2018); NOF Corporation (Japan) (2018); Winthrop Rockefeller Foundation (2024–2026); Shanghai First People's Hospital (2018); Second Affiliated Hospital of Nanjing Medical University (2021–2023); Proteome Sciences (United Kingdom) (2018); First Affiliated Hospital of Zhengzhou University (2024–2026); Hangzhou Children's Hospital (2024); Baoding People's Hospital (2025); Hebei University (2022); Zhejiang University of Technology (2025); Southern Medical University (2019); Ocean University of China (2016); Southeast University (2022–2023); Henan Medical University (2018); Nanjing Medical University (2021–2025)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Jiaojiao Fan's research focuses on the molecular mechanisms underlying kidney diseases and the development of therapeutic strategies. Fan has investigated the role of the protein LONP1 in protecting mitochondrial function to attenuate chronic kidney disease and explored how the anti-anemia drug FG4592 may retard the transition from acute kidney injury to chronic kidney disease by enhancing vascular regeneration and antioxidative capabilities. Further work has examined the therapeutic potential of targeting podocyte mitochondrial dysfunction in focal segmental glomerulosclerosis and the role of TP53RK in driving chronic kidney disease progression. Fan also studies the impact of hypoxia-inducible factor prolyl hydroxylase inhibitors in nonanemic diseases and the protective effects of novel compounds against acute kidney injury. Additionally, Fan has published on the DNA damage response induced by the human endogenous retrovirus type K encoded Np9 oncoprotein. Fan's scholarship metrics include an h-index of 13, with 66 total publications and 591 citations.
Metrics
- h-index: 13
- Publications: 68
- Citations: 604
Selected Publications
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Mitochondrial-targeted SS-31 peptide attenuates radiation-induced cardiomyocyte senescence (2026)
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Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence (2026)
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Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation (2026)
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Targeting Hyaluronan Signaling Overcomes Primary Effusion Lymphoma Cells Resistance to Rapamycin (2026)
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Roles of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway in Oncovirus Infection and Virus-Associated Cancers (2025)
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Infection of human induced pluripotent stem cells by an oncogenic herpesvirus (2025)
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Identification of RP‐54745, an IL‐1 Inhibitor Displaying Anticancer Activities for KSHV‐Related Primary Effusion Lymphoma (2025)
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Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity (2024)
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SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence (2024)
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Roles of Human Endogenous Retrovirus-K-Encoded Np9 in Human Diseases: A Small Protein with Big Functions (2024)
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Human endogenous retrovirus type K encoded Np9 oncoprotein induces DNA damage response (2024)
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Development of human endogenous retrovirus type K‐ related treatments for human diseases (2024)
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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
- Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity
- Identification of RP‐54745, an IL‐1 Inhibitor Displaying Anticancer Activities for KSHV‐Related Primary Effusion Lymphoma
Showing 5 of 6 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
- 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
- Roles of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway in Oncovirus Infection and Virus-Associated Cancers
- 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 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
- 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
- Mitochondrial proton leak in cardiac aging
- Mitochondrial proton leak in cardiac aging
- 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
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Alterations in Cellular Gene Expression Due to Co‐Infection With Kaposi's Sarcoma‐Associated Herpesvirus and SARS‐CoV‐2: Implications for Disease Severity
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