Wenduo Liu

Dr. Wenduo Liu

orcid

Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2024 in Aging and disease
Verified
Journal Article
Open access
PDF file
ZWZilin Wang
Zilin Wang
HSHyun-Jaung Sim
Hyun-Jaung Sim
WLWenduo Liu
Wenduo Liu
JKJae Cheol Kim
Jae Cheol Kim
JLJeong-Chae Lee
Jeong-Chae Lee
SKSang Hyun Kim
Sang Hyun Kim
One of the most important strategies for successful aging is exercise. However, the effect of exercise can differ among individuals, even with exercise of the same type and intensity. Therefore, this study aims to confirm whether endurance training (ETR) has the same health-promoting effects on the musculoskeletal and hematopoietic systems regardless of age. Ten weeks of ETR improved endurance exercise capacity, with increased skeletal muscle mitochondrial enzymes in both young and old mice. In addition, age-related deterioration of muscle fiber size and bone microstructure was improved. The expression levels of myostatin, muscle RING-finger protein-1, and muscle atrophy F-box in skeletal muscle and peroxisome proliferator-activated receptor-γ in the femur increased with age but decreased after ETR. ETR differentially modulated hematopoietic stem cells (HSCs) depending on age; ETR induced HSC quiescence in young mice but caused HSC senescence in old mice. ETR has differential effects on modulation of the musculoskeletal and hematopoietic systems in old mice. In other words, endurance exercise is a double-edged sword for successful aging, and great effort is required to establish exercise strategies for healthy aging.

4 June 2025 in Frontiers in Public Health
Verified
Journal Article
Open access
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YDYi Ding
Yi Ding
QWQiliang Wan
Qiliang Wan
WLWenduo Liu
Wenduo Liu
This study aims to explore the multifaceted impacts and mechanisms of fine particulate matter (PM2.5) exposure on skeletal muscle mitochondria. Evidence suggests that PM2.5 can penetrate the respiratory barrier and enter the circulatory system, spreading throughout the body and causing significant damage to the morphology, quantity, and function of skeletal muscle mitochondria. This is manifested by a decline in oxidative phosphorylation efficiency and mitochondrial dysfunction. Meanwhile, PM2.5 exposure induces excessive production of reactive oxygen species, triggering oxidative stress responses that impair mitochondrial dynamic regulation. This further disrupts the balance of glucose and lipid metabolism in skeletal muscle, exacerbating the development of metabolic diseases. The review underscores the systemic effects on skeletal muscle following mitochondrial dysfunction after PM2.5 exposure and the preventive and treatment potential of exercise.

1 November 2024 in The Korean Journal of Physiology & Pharmacology
Verified
Journal Article
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YGYu Gu
Yu Gu
DSDong-Hun Seong
Dong-Hun Seong
WLWenduo Liu
Wenduo Liu
ZWZilin Wang
Zilin Wang
YJYong Whi Jeong
Yong Whi Jeong
SKSang Hyun Kim
Sang Hyun Kim
Yu Gu, Dong-Hun Seong, Wenduo Liu, Zilin Wang, Yong Whi Jeong, Jae-Cheol Kim, Dae Ryong Kang, Rose Ji Eun Lee, Jin-Ho Koh, and Sang Hyun Kim. Korean J Physiol Pharmacol 2024;28:515-26. https://doi.org/10.4196/kjpp.2024.28.6.515

28 February 2024 in Frontiers in Public Health
Verified
Journal Article
Open access
PDF file
WLWenduo Liu
Wenduo Liu
ZWZilin Wang
Zilin Wang
YGYu Gu
Yu Gu
HSHan-Sol So
Han-Sol So
SKSung-Ho Kook
Sung-Ho Kook
SKSang Hyun Kim
Sang Hyun Kim
Introduction: This study aimed to investigate the potential of short-term aerobic exercise to mitigate skeletal muscle mitochondrial damage following ambient PM2.5 exposure, and how 12 weeks of endurance training can enhance aerobic fitness to protect against such damage.Methods: Twenty-four male C57BL/6 J mice were split into sedentary (SED, n = 12) and endurance training (ETR, n = 12) groups. The ETR group underwent 12 weeks of training (10–15 m/min, 60 min/day, 4 times/week), confirmed by an Endurance Exercise Capacity (EEC) test. Post-initial training, the SED group was further divided into SSED (SED and sedentary, n = 6) and SPE (SED and PM2.5 + Exercise, n = 6). Similarly, the ETR group was divided into EEX (ETR and Exercise, n = 6) and EPE (ETR and PM2.5 + Exercise, n = 6). These groups underwent 1 week of atmospherically relevant artificial PM2.5 exposure and treadmill running (3 times/week). Following treatments, an EEC test was conducted, and mice were sacrificed for blood and skeletal muscle extraction. Blood samples were analyzed for oxidative stress indicators, while skeletal muscles were assessed for mitochondrial oxidative metabolism, antioxidant capacity, and mitochondrial damage using western blot and transmission electron microscopy (TEM).Results: After 12 weeks of endurance training, the EEC significantly increased (p < 0.000) in the ETR group compared to the SED group. Following a one-week comparison among the four groups with atmospherically relevant artificial PM2.5 exposure and exercise treatment post-endurance training, the EEX group showed improvements in EEC, oxidative metabolism, mitochondrial dynamics, and antioxidant functions. Conversely, these factors decreased in the EPE group compared to the EEX. Additionally, within the SPE group, exercise effects were evident in HK2, LDH, SOD2, and GPX4, while no impact of short-term exercise was observed in all other factors. TEM images revealed no evidence of mitochondrial damage in both the SED and EEX groups, while the majority of mitochondria were damaged in the SPE group. The EPE group also exhibited damaged mitochondria, although significantly less than the SPE group.Conclusion: Atmospherically relevant artificial PM2.5 exposure can elevate oxidative stress, potentially disrupting the benefits of short-term endurance exercise and leading to mitochondrial damage. Nonetheless, increased aerobic fitness through endurance training can mitigate PM2.5-induced mitochondrial damage.

26 September 2025 in Frontiers in Physiology
Verified
Journal Article
Open access
PDF file
YDYi Ding
Yi Ding
QWQiliang Wan
Qiliang Wan
JKJae Cheol Kim
Jae Cheol Kim
WLWenduo Liu
Wenduo Liu
WJWeiping Ji
Weiping Ji
Background: Skeletal muscle aging is often accompanied by capillary rarefaction, which limits the effective delivery and distribution of hormones, nutrients, and growth factors within skeletal muscle. Furthermore, exercise is widely regarded as having the potential to improve microcirculation and delay skeletal muscle aging. This review aims to explore exercise-induced improvements in capillarization and related adaptations to mitigate the adverse changes that occur during the aging process of skeletal muscle.Methods: This systematic review was conducted in accordance with the PRISMA guidelines and registered in the PROSPERO database under the identifier CRD420251055873. Studies involving exercise interventions in older adults were included, with the requirement that at least one original outcome related to skeletal muscle capillarization was reported. Articles were rigorously screened based on the PICOS criteria, and the quality of the included studies was assessed.Results: Studies have shown that older adults still possess the capacity to improve skeletal muscle capillarization through exercise. Moderate-intensity aerobic exercise not only significantly enhances the level of capillarization but also induces effects that can be maintained even after cessation of training. Capillarization adaptations induced by resistance training exhibit marked inter-individual variability, which is primarily determined by each individual’s baseline level of capillarization, thereby resulting in distinct patterns of adaptation. The studies also revealed that the regulation of capillarization depends on the synergistic action of VEGF and eNOS, and that different types of exercise may elicit adaptations through distinct molecular pathways.Conclusion: During the aging process, exercise-induced improvements in capillarization can enhance nutrient delivery, metabolic efficiency, and regenerative capacity in skeletal muscle. To some extent, these adaptations help suppress degenerative changes in muscle function and provide a targeted foundation for anti-aging intervention strategies.

8 September 2025 in Frontiers in Sports and Active Living
Verified
Journal Article
Open access
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YZYinping Zeng
Yinping Zeng
WJWeiguo Ji
Weiguo Ji
YSYu Shi
Yu Shi
WLWenduo Liu
Wenduo Liu
WJWeiping Ji
Weiping Ji
Elite football players are particularly vulnerable to sports injuries due to the demands of high-intensity training and competition, which negatively affect their athletic careers and the economic interests of their clubs. Currently, the structural classification of injury scenarios and types in football remains unclear, hindering players' understanding of injuries and the implementation of effective preventive measures. This study aims to refine the structural classification of football-related injuries and update the corresponding scenarios, prevention strategies, and treatment approaches for general sports injuries, degenerative injuries, and accidental injuries. Researchers screened relevant literature from PubMed, SportDiscus, and Google Scholar databases from May 2000 to May 2025. For general sports injuries, skeletal muscle injuries (muscle fiber injuries, tendon injuries) can be prevented through eccentric strength training, while joint injuries (ligament injuries, muscle imbalances) require a focus on neuromuscular control training. Degenerative injuries necessitate systematic treatment, and surgical intervention should be adopted, when necessary, followed by a personalized rehabilitation program. Accidental injuries (concussions and fractures) can be mitigated using protective gear, rule modifications, and enhanced safety measures education. This article emphasizes the importance of a structured classification system for injury prevention and differentiated treatment strategies for elite football players. This will provide a theoretical basis for establishing clear understanding among individual athletes and reducing the occupational risk of injury in football.