L. Teng — Researcher Analysis Report
Analysis Mode: fast | Analysis Time: 2026-03-16T00:17:54
Rating: Active Researcher (45.5/100)
Basic Metrics
| Metric | Value |
|---|---|
| Institution | Unknown |
| h-index | 21 |
| Total Citations | 1,607 |
| Recent 5 Years Citations | 63 |
| Total Papers | 55 |
| Papers in Top Conferences | 0 |
| Publication Period | 2008 - 2025 |
| Semantic Scholar | 49286689 |
Research Trajectory
L. Teng’s academic trajectory exhibits high fragmentation, with papers spanning unrelated fields such as glioma treatment, cardiac stem cells, NADPH oxidase vascular biology, immunology of marine model organisms, and GaAs quantum well spin relaxation. This strongly suggests that the authorship is a combination of multiple researchers (name duplication issue). Focusing on his main research line, a core research theme centered on glioma diagnosis and treatment can be identified: entering this field in 2011 with a review titled “Aberrant Signaling Pathways in Glioma” (219 citations), and publishing several high-impact mechanistic studies between 2011–2013 regarding 5-ALA fluorescence-guided surgery and photodynamic therapy, which constitute the main source of his academic influence.
The key turning point in his career trajectory occurred during the intensive period from 2011–2013—by revealing the regulatory mechanism of ferrochelatase silencing and ABCB6 over-expression in porphyrin IX accumulation, he provided a molecular target for improving the quality of clinical 5-ALA fluorescence surgery. Three representative works have received more than 450 citations in total. However, the number of citations in the past 5 years is only 63 (out of 1,607 over his career), indicating that his research influence has significantly declined after 2018, and his new research directions have become more dispersed (C-phycocyanin, zebrafish, SGLT-2), failing to establish a continuous core research framework.
Breakthrough Works
1. Aberrant Signaling Pathways in Glioma (2011)
Description: A systematic review of the abnormal activation mechanisms of key signaling pathways such as EGFR, PDGFR, PTEN/PI3K/Akt, Rb/CDK4, and p53 in glioblastoma (GBM), providing a theoretical framework for targeted therapy strategies.
Why it couldn’t be done before: The accumulation of key insights required time: after the release of the TCGA glioma genome map data in 2007, researchers were able to systematically integrate the full picture of multi-pathway abnormalities; prior research on each pathway was relatively isolated, lacking a cross-pathway integrated perspective.
Impact: It became a highly cited review in the field of glioma signaling pathways (219 times), providing a standard reference framework for subsequent targeted drug development and combination therapy strategies.
2. Silencing of ferrochelatase enhances 5-aminolevulinic acid-based fluorescence and photodynamic therapy efficacy (2011)
Description: It was discovered that silencing ferrochelatase (FECH) can block the metabolic conversion of PpIX to hemoglobin, thereby significantly enhancing the fluorescence intensity and photodynamic therapeutic effect of 5-ALA in glioma cells.
Why it couldn’t be done before: Clinical 5-ALA fluorescence surgery has been used for many years, but insufficient PpIX accumulation limited the fluorescence quality. The breakthrough of this work lies in identifying FECH as a key metabolic bottleneck—detailed enzymatic maps of the 5-ALA metabolism pathway and mature siRNA gene silencing technology were only available around 2010.
Impact: 158 citations, opening up a research direction to improve 5-ALA fluorescence quality through metabolic intervention, providing an operable target for optimizing clinical fluorescence-guided surgery.
3. Increased Expression of ABCB6 Enhances Protoporphyrin IX Accumulation and Photodynamic Effect in Human Glioma (2013)
Description: It was revealed that over-expression of ATP-binding cassette protein ABCB6 promotes PpIX accumulation in mitochondria, enhancing the photodynamic therapy sensitivity of glioma from another mechanism perspective.
Why it couldn’t be done before: The understanding of ABCB6’s function in porphyrin transport was only initially established in 2009; linking it to enhanced PDT sensitivity in glioma required integration of cross-disciplinary knowledge (mitochondrial transport biology + tumor photodynamic therapy), which had not been accomplished before.
Impact: 98 citations, together with the ferrochelatase study, constructed a dual-target strategy for regulating PpIX metabolism, driving a research boom in the mechanism of glioma photodynamic therapy.
4. The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release (2012)
Description: For the first time, it was demonstrated that HO-1 inducer CoPP can increase the survival rate after human cardiac stem cell (hCSC) transplantation through the ERK/NRF2 pathway and cytokine release, addressing the core obstacle of high cell death rates in stem cell therapy.
Why it couldn’t be done before: The clinical translational potential of c-kit+ cardiac stem cells was confirmed only in 2003, and their extremely low survival rate (>90% die within 7 days) became a bottleneck. Applying the cellular protection mechanism of HO-1/CO system to pre-treatment of cardiac stem cells required systematic integration of knowledge from two separate fields (HO-1 cardiovascular protection and stem cell therapy).
Impact: 97 citations, establishing the combined strategy of “pre-treatment + stem cell transplantation” and driving research directions in cellular survival in cardiac regenerative medicine.
5. The synergistic antitumor effects of all-trans retinoic acid and C-phycocyanin on the lung cancer A549 cells in vitro and in vivo (2015)
Description: In in vitro and in vivo models, it was confirmed that all-trans retinoic acid (ATRA) and C-phycocyanin together have a synergistic antitumor effect on lung cancer A549 cells, providing experimental evidence for natural product combination differentiation-induced therapy.
Why it couldn’t be done before: The anti-tumor mechanism of C-phycocyanin was gradually elucidated in the early 2010s; combining it with mature ATRA differentiation therapy required cross-study research on both mechanisms, and data accumulation until around 2015 was insufficient for systematic combined research.
Impact: 86 citations, one of the landmark studies in the application of C-phycocyanin in antitumor therapy, driving exploration of this natural pigment in tumor pharmacology.
Research Directions
- Glioma diagnosis and treatment (optimization of 5-ALA fluorescence-guided surgery mechanism, enhanced PDT sensitivity, targeted therapy via signaling pathways, glioma stem cells)
- Cardiac stem cells and myocardial protection (HO-1/NO pre-treatment strategies, ERK/NRF2 survival pathways)
- NADPH oxidase and endothelial cell oxidative stress (p47phox phosphorylation regulation mechanism)
- Immunology and developmental biology of marine/zebrafish model organisms (defensins, Ly6 family, MOV10, CD248)
Methodological Evolution
Early period (2008–2010) relied mainly on classical molecular biology methods: western blot, gene knockout mouse models, protein phosphorylation analysis, primarily studying the regulatory mechanism of NADPH oxidase. From 2011–2014, the methodology reached maturity, introducing RNAi gene silencing, fluorescence microscopy imaging, in vitro and in vivo photodynamic therapy models. Experimental design shifted from single-molecule mechanisms to full-chain validation of “target → intervention → functional phenotype,” driving the production of highly influential papers. After 2015, the methodology became significantly fragmented: on one hand, in vivo tumor models continued; on the other hand, completely different methodological systems such as zebrafish development models, phylogenetic analysis, and reproductive toxicology tests were introduced, indicating a lack of sustained focus on research directions. In recent years (2024–2025), clinical observational studies shifted toward cardiac clinical reviews, with almost no methodological continuity from early basic research.
Field Impact
In the niche field of glioma 5-ALA metabolism regulation, L. Teng (as a core researcher in glioma) made substantial contributions: through the discovery of two complementary mechanism targets—ferrochelatase and ABCB6—he systematically elucidated the metabolic network affecting PpIX accumulation, which was frequently cited by subsequent research in this field. The h-index = 21 mainly stems from this period. However, due to the lack of focus on the main research line after 2017, no continuous research framework was formed around 5-ALA surgery optimization or glioma targeted therapy, missing the window for advancing early mechanism discoveries into clinical translation. Overall assessment: a valuable contributor in a specific niche rather than a leading figure in the field; the significant decline in influence in the past 5 years (only 63 citations) indicates that his academic influence has entered a plateau phase.
Top 20 Citations Papers| # | Year | Citation | Title |
|—|——|——|——| | 1 | 2011 | 219 | Aberrant Signaling Pathways in Glioma | | 2 | 2011 | 158 | Silencing of ferrochelatase enhances 5-aminolevulinic acid-based fluorescence and photodynamic therapy efficacy | | 3 | 2013 | 98 | Increased Expression of ABCB6 Enhances Protoporphyrin IX Accumulation and Photodynamic Effect in Human Glioma | | 4 | 2012 | 97 | The Heme Oxygenase 1 Inducer (CoPP) Protects Human Cardiac Stem Cells against Apoptosis through Activation of the Extracellular Signal-regulated Kinase (ERK)/NRF2 Signaling Pathway and Cytokine Release* | | 5 | 2015 | 86 | The synergistic antitumor effects of all-trans retinoic acid and C-phycocyanin on the lung cancer A549 cells in vitro and in vivo. | | 6 | 2013 | 70 | Glycogen synthase kinase 3β inhibition sensitizes human glioblastoma cells to temozolomide by affecting O6-methylguanine DNA methyltransferase promoter methylation via c-Myc signaling. | | 7 | 2011 | 63 | A miR-21 inhibitor enhances apoptosis and reduces G2-M accumulation induced by ionizing radiation in human glioblastoma U251 cells | | 8 | 2009 | 56 | Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase | | 9 | 2015 | 40 | Preconditioning Human Cardiac Stem Cells with an HO‐1 Inducer Exerts Beneficial Effects After Cell Transplantation in the Infarcted Murine Heart | | 10 | 2017 | 36 | Identification of antipsychotic drug fluspirilene as a potential anti-glioma stem cell drug | | 11 | 2012 | 32 | The first chordate big defensin: identification, expression and bioactivity. | | 12 | 2013 | 32 | Ligand-dependent EphB1 signaling suppresses glioma invasion and correlates with patient survival. | | 13 | 2013 | 32 | Combination therapy using Notch and Akt inhibitors is effective for suppressing invasion but not proliferation in glioma cells. | | 14 | 2020 | 32 | Interfering with hyaluronic acid metabolism suppresses glioma cell proliferation by regulating autophagy | | 15 | 2018 | 29 | P68 RNA helicase promotes invasion of glioma cells through negatively regulating DUSP5 | | 16 | 2012 | 26 | Divergent Effects of p47phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-&agr; Signaling via TRAF4 and MAPK in Endothelial Cells | | 17 | 2016 | 26 | Preconditioning c-Kit-positive Human Cardiac Stem Cells with a Nitric Oxide Donor Enhances Cell Survival through Activation of Survival Signaling Pathways* | | 18 | 2009 | 24 | Knockout of p47phox Uncovers a Critical Role of p40phox in Reactive Oxygen Species Production in Microvascular Endothelial Cells | | 19 | 2014 | 24 | Calcitriol enhances 5-aminolevulinic acid-induced fluorescence and the effect of photodynamic therapy in human glioma | | 20 | 2017 | 21 | NRG-1β exerts neuroprotective effects against ischemia reperfusion-induced injury in rats through the JNK signaling pathway. |