Ke Ning

Dr. Ke Ning

College of Exercise and Health, Shenyang Sport University, Shenyang, Liaoning, China

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

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

Representative Publications

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25 September 2024 in Biomolecules
Verified
Journal Article
Open access
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ZLZheng Lu
Zheng Lu
ZWZhuo Wang
Zhuo Wang
ZXzhang xinan
zhang xinan
KNKe Ning
Ke Ning
Exercise can regulate the immune function, activate the activity of immune cells, and promote the health of the organism, but the mechanism is not clear. Skeletal muscle is a secretory organ that secretes bioactive substances known as myokines. Exercise promotes skeletal muscle contraction and the expression of myokines including irisin, IL-6, BDNF, etc. Here, we review nine myokines that are regulated by exercise. These myokines have been shown to be associated with immune responses and to regulate the proliferation, differentiation, and maturation of immune cells and enhance their function, thereby serving to improve the health of the organism. The aim of this article is to review the effects of myokines on intrinsic and adaptive immunity and the important role that exercise plays in them. It provides a theoretical basis for exercise to promote health and provides a potential mechanism for the correlation between muscle factor expression and immunity, as well as the involvement of exercise in body immunity. It also provides the possibility to find a suitable exercise training program for immune system diseases.

19 August 2022 in Frontiers in Aging Neuroscience
Verified
Journal Article
Open access
KNKe Ning
Ke Ning
ZWZhuo Wang
Zhuo Wang
ZXzhang xinan
zhang xinan
Osteoarthritis is a chronic degenerative musculoskeletal disease characterized by pathological changes in joint structures along with the incidence of which increases with age. Exercise is recommended for all clinical treatment guidelines of osteoarthritis, but the exact molecular mechanisms are still unknown. Irisin is a newly discovered myokine released mainly by skeletal muscle in recent years—a biologically active protein capable of being released into the bloodstream as an endocrine factor, the synthesis and secretion of which is specifically induced by exercise-induced muscle contraction. Although the discovery of irisin is relatively recent, its role in affecting bone density and cartilage homeostasis has been reported. Here, we review the production and structural characteristics of irisin and discuss the effects of the different types of exercise involved in the current study on irisin and the role of irisin in anti-aging. In addition, the role of irisin in the regulation of bone mineral density, bone metabolism, and its role in chondrocyte homeostasis and metabolism is reviewed. A series of studies on irisin have provided new insights into the mechanisms of exercise training in improving bone density, resisting cartilage degeneration, and maintaining the overall environmental homeostasis of the joint. These studies further contribute to the understanding of the role of exercise in the fight against osteoarthritis and will provide an important reference and aid in the development of the field of osteoarthritis prevention and treatment.

6 August 2020 in Cancer Science
Verified
Journal Article
Open access
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KNKe Ning
Ke Ning
YSYangguang Shao
Yangguang Shao
YHYuxin He
Yuxin He
FWFei Wang
Fei Wang
XCXi Cui
Xi Cui
FLFeng Li
Feng Li
The histone demethylase Jumonji domain‐containing 1A (JMJD1A) is overexpressed in multiple cancers and promotes cancer progression. However, the role and mechanism of JMJD1A in gastric cancer (GC) remains poorly understood. Here, we found that JMJD1A could suppress GC cell proliferation and xenograft tumor growth. Using RNA sequencing, we identified runt‐related transcription factor 3 (RUNX3) as a novel target gene of JMJD1A. Mechanistically, we identified that JMJD1A upregulated RUNX3 through co–activating Ets‐1 and reducing the H3K9me1/2 levels at the RUNX3 promoter in GC cells. Functionally, JMJD1A inhibits the growth of GC cells in vivo, which is partially dependent on RUNX3. Moreover, JMJD1A expression was decreased in GC and low expression of JMJD1A was correlated with an aggressive phenotype and a poor prognosis in patients with GC. Importantly, JMJD1A expression was positively associated with RUNX3 expression in GC samples. These studies indicated that JMJD1A upregulates RUNX3 expression via co–activation of transcription factor Ets‐1 to inhibit proliferation of GC cells. Our findings provide new insight into the mechanism by which JMJD1A regulates RUNX3 transcription and suggest that JMJD1A and/or RUNX3 may be used as a therapeutic intervention for GC.