Zhenyu Liu
Research Subjects
Zhenyu Liu has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Yaqi Zhai
Department of Gastroenterology, The First Medical Center of Chinese PLA General Hospital, Beijing, China
3 shared publications - Enqiang Linghu
Department of Gastroenterology and Hepatology, The First Medical Centre, Chinese PLA General Hospital, Beijing, People’s Republic of China
2 shared publications - Jian Cong Feng
Department of Gastroenterology The First Medical Center of Chinese PLA General Hospital Beijing China
2 shared publications - Ammara Safdar
Beijing Key Laboratory for Drug Delivery Nanocarriers, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing 100190, China
1 shared publication - Bozhao Li
Beijing Key Laboratory for Drug Delivery Nanocarriers, CAS Center for Excellence in Nanoscience, National Center for Nanoscience and Technology, Beijing 100190, China
1 shared publication Dandan Li
Department of Transfusion Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China
1 shared publication
Latest Publications
- Open Access
- 8 July 2026
- Published by AVES YAYINCILIK A.Ş. in Turkish Journal of Gastroenterology
- Vol. 37 (8) , 912-914
A Simple and Effective Method for Endoscopic Fragmentation of Gastric Bezoars
Cite this article as: Liang H, Yin T, Liu Z. A simple and effective method for endoscopic fragmentation of gastric bezoars. Turk J Gastroenterol. Published online June 8, 2026. doi: 10.5152/tjg.2026.26208.
- 8 July 2026
- Published by AVES YAYINCILIK A.Ş. in Turkish Journal of Gastroenterology
- Vol. 37 (8) , 912-914
Open AccessA Simple and Effective Method for Endoscopic Fragmentation of Gastric Bezoars
Cite this article as: Liang H, Yin T, Liu Z. A simple and effective method for endoscopic fragmentation of gastric bezoars. Turk J Gastroenterol. Published online June 8, 2026. doi: 10.5152/tjg.2026.26208.
- 1 July 2026
- Published by Wiley in Journal of Digestive Diseases
- Vol. 27 (7-8) , 342-348
A Novel Endoscopic Suture Anchor ( ESA ) Device for Full‐Thickness Defect Closure: A Comprehensive Ex Vivo and In Vivo Evaluation (With Video)
Objectives: A novel endoscopic suture anchor (ESA) device has been developed based on the through‐the‐scope clip (TTSC) system. We conducted this preclinical study aiming to comprehensively evaluate its feasibility, safety, and efficacy for full‐thickness defect closure. Methods: Ex vivo porcine stomachs ( n = 11) and in vivo Bama porcine models ( n = 8) were used. Endoscopic full‐thickness resection (EFTR) was performed to create an artificial gastric defect, followed by defect closure using the ESA devices. The primary outcome was the closure success rate. Secondary outcomes included the technical success rate, biomechanical testing results (leakage pressure, static tensile force, and pull‐out force), closure time, complete healing rate, and incidence of adverse events (AEs). Results: In ex vivo models, both the closure and technical success rates were 90.9%, with one case of suture breakage. The mean leakage pressure, static tensile force, and pull‐out force were (20.67 ± 3.20) mmHg, (4.75 ± 0.60) N, and (9.27 ± 3.42) N, respectively. In in vivo porcine models, both the closure and technical success rates reached 100%. The mean closure time was (18.75 ± 3.99) min. Complete healing was confirmed in all animals by endoscopic and histopathological assessments at the scheduled end‐points, without AEs. Conclusion: ESA is feasible, safe, and effective for gastric full‐thickness defect closure and could be a promising device in clinical practice.
- 1 July 2026
- Published by Wiley in Journal of Digestive Diseases
- Vol. 27 (7-8) , 342-348
A Novel Endoscopic Suture Anchor ( ESA ) Device for Full‐Thickness Defect Closure: A Comprehensive Ex Vivo and In Vivo Evaluation (With Video)
Objectives: A novel endoscopic suture anchor (ESA) device has been developed based on the through‐the‐scope clip (TTSC) system. We conducted this preclinical study aiming to comprehensively evaluate its feasibility, safety, and efficacy for full‐thickness defect closure. Methods: Ex vivo porcine stomachs ( n = 11) and in vivo Bama porcine models ( n = 8) were used. Endoscopic full‐thickness resection (EFTR) was performed to create an artificial gastric defect, followed by defect closure using the ESA devices. The primary outcome was the closure success rate. Secondary outcomes included the technical success rate, biomechanical testing results (leakage pressure, static tensile force, and pull‐out force), closure time, complete healing rate, and incidence of adverse events (AEs). Results: In ex vivo models, both the closure and technical success rates were 90.9%, with one case of suture breakage. The mean leakage pressure, static tensile force, and pull‐out force were (20.67 ± 3.20) mmHg, (4.75 ± 0.60) N, and (9.27 ± 3.42) N, respectively. In in vivo porcine models, both the closure and technical success rates reached 100%. The mean closure time was (18.75 ± 3.99) min. Complete healing was confirmed in all animals by endoscopic and histopathological assessments at the scheduled end‐points, without AEs. Conclusion: ESA is feasible, safe, and effective for gastric full‐thickness defect closure and could be a promising device in clinical practice.
- 3 June 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Translational Medicine
- Vol. 18 (852) , eaea0189
Reprogrammed apoptotic platelets drive rapid hemostasis through phosphatidylserine and prostaglandin E2 signaling in preclinical models
Uncontrolled hemorrhage in trauma, surgical, organ-related, and endoscopic settings, particularly in patients receiving antiplatelet therapy, remains difficult to manage clinically. Here, we introduce a high phosphatidylserine (PS)–exposed procoagulant platelet (hPPL) derivative reprogrammed from isolated platelets via calcium ionophore A23187–induced apoptosis, enriched in surface PS and capable of driving rapid hemostasis. Retaining a protein profile akin to resting platelets, hPPLs robustly promoted platelet activation and aggregation in human- and rat-derived plasma and whole blood in vitro and demonstrated superior hemostatic efficacy compared with clinical thrombin and commercial hemostatic materials [microporous polysaccharide hemispheres (MPH) and FIBRILLAR] in murine liver injury and porcine gastric ulcer bleeding models, even under antiplatelet treatment. Mechanistically, hPPLs up-regulated prostaglandin E synthase (PTGES), thereby increasing prostaglandin E2 (PGE 2 ) production and its receptor 3 (EP3)–mediated platelet activation, which reinforced PS-mediated clot formation. Our findings identified an apoptosis-driven PTGES-PGE 2 -EP3 signaling axis that augmented PS-mediated coagulation in murine and porcine hemorrhage models and established the hPPL derivative as a topical hemostatic agent with translational potential for organ-related bleeding and distinct advantages in managing complex endoscopic hemorrhages under both physiological and coagulopathic conditions.
- 3 June 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Translational Medicine
- Vol. 18 (852) , eaea0189
Reprogrammed apoptotic platelets drive rapid hemostasis through phosphatidylserine and prostaglandin E2 signaling in preclinical models
Uncontrolled hemorrhage in trauma, surgical, organ-related, and endoscopic settings, particularly in patients receiving antiplatelet therapy, remains difficult to manage clinically. Here, we introduce a high phosphatidylserine (PS)–exposed procoagulant platelet (hPPL) derivative reprogrammed from isolated platelets via calcium ionophore A23187–induced apoptosis, enriched in surface PS and capable of driving rapid hemostasis. Retaining a protein profile akin to resting platelets, hPPLs robustly promoted platelet activation and aggregation in human- and rat-derived plasma and whole blood in vitro and demonstrated superior hemostatic efficacy compared with clinical thrombin and commercial hemostatic materials [microporous polysaccharide hemispheres (MPH) and FIBRILLAR] in murine liver injury and porcine gastric ulcer bleeding models, even under antiplatelet treatment. Mechanistically, hPPLs up-regulated prostaglandin E synthase (PTGES), thereby increasing prostaglandin E2 (PGE 2 ) production and its receptor 3 (EP3)–mediated platelet activation, which reinforced PS-mediated clot formation. Our findings identified an apoptosis-driven PTGES-PGE 2 -EP3 signaling axis that augmented PS-mediated coagulation in murine and porcine hemorrhage models and established the hPPL derivative as a topical hemostatic agent with translational potential for organ-related bleeding and distinct advantages in managing complex endoscopic hemorrhages under both physiological and coagulopathic conditions.
- Open Access
- 31 October 2025
- Published by AVES YAYINCILIK A.Ş. in Turkish Journal of Gastroenterology
- Vol. 37 (1) , 136-138
Novel Endoscopic Suture Anchor Device for Large Defect Closure Following Endoscopic Submucosal Dissection
Cite this article as: Feng J, Zhai Y, Liu Z, Linghu E. Novel endoscopic suture anchor device for large defect closure following endoscopic submucosal dissection. Turk J Gastroenterol. Published online October 31, 2025. doi:10.5152/tjg.2025.25240
- 31 October 2025
- Published by AVES YAYINCILIK A.Ş. in Turkish Journal of Gastroenterology
- Vol. 37 (1) , 136-138
Open AccessNovel Endoscopic Suture Anchor Device for Large Defect Closure Following Endoscopic Submucosal Dissection
Cite this article as: Feng J, Zhai Y, Liu Z, Linghu E. Novel endoscopic suture anchor device for large defect closure following endoscopic submucosal dissection. Turk J Gastroenterol. Published online October 31, 2025. doi:10.5152/tjg.2025.25240