1d
2
2
20
5
5
1e
5
1d
19a
c
27
1a
3f
21
c
1c
15
2
7
15
5
21
5
3
6
17
4
4
2
22
3
1a
4
8
1c
c
3
4e
16
9
c
19
1
49
2
6
d
1b
1d
18
79
2f
1d
2 29
1d
25
2f
Fanxin Long, Ph.D.
45Professor of Orthopaedic Surgery
7
6a
Department: Orthopaedic Surgery
4
1
23
1f
Graduate Group Affiliations
8
a
b
1d
46
Contact information
74
4
3
3
1d
74
The Children's Hospital of Philadelphia, Abramson Research Center 902A
39 3615 Civic Center Blvd
Philadelphia, PA 19104
26
39 3615 Civic Center Blvd
Philadelphia, PA 19104
35
7f
Email:
longf1@chop.edu
12
longf1@chop.edu
18
Publications
23 a
3
2
4
b
1f
23 a
13
Education:
21 9 B.S. 19 (Cell Biology) c
2a Peking University, 1988.
21 9 M.A. 2f (Biochemistry and Molecular Biology) c
40 University of California, Santa Barbara, 1992.
21 a Ph.D. 22 (Developmental Biology) c
3c Tufts University School of Medicine, 1997.
c
3
27
21 9 B.S. 19 (Cell Biology) c
2a Peking University, 1988.
21 9 M.A. 2f (Biochemistry and Molecular Biology) c
40 University of California, Santa Barbara, 1992.
21 a Ph.D. 22 (Developmental Biology) c
3c Tufts University School of Medicine, 1997.
c
Links
e1 Search PubMed for articles
d
5
21
e1 Search PubMed for articles
d
1f
Post-Graduate Training
24 75 Postdoctoral Fellow in Cell Biology, Harvard Medical School, Department of Cell Biology, 1997-1999.
24 95 Postdoctoral Fellow in Molecular and Cellular Biology, Harvard University, Department of Molecular and Cellular Biology, 1999-2002.
c
3
3
8d
Permanent link24 75 Postdoctoral Fellow in Cell Biology, Harvard Medical School, Department of Cell Biology, 1997-1999.
24 95 Postdoctoral Fellow in Molecular and Cellular Biology, Harvard University, Department of Molecular and Cellular Biology, 1999-2002.
c
2 29
21
1e
1d
24
76
9d The Long lab seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone disorders.
8
11 Key Words
c3 mesenchymal stem/progenitor cells, metabolic and epigenetic regulation, skeletal cell differentiation and function, diabetic osteopenia, skeletal aging, bone development and regeneration
8
18 Research Details
520 Skeletal diseases, ranging from congenital dysplasia to osteosarcoma to osteoarthritis and osteoporosis, take a significant toll on human health. The overarching goal of our research is to discover key steps in the molecular or metabolic regulation of skeletal cell differentiation or function, with the hope of uncovering therapeutic targets for treating the various skeletal diseases. Many of our studies have centered around the role and mechanism of key developmental signals such as Hh, Wnt, Notch and Bmp in regulating skeletal development and homeostasis. Through mouse genetic studies, we have defined specific functions of the developmental signals in bone and cartilage cell differentiation. Our molecular and biochemical studies have led to the discovery that the developmental signals alter cell fate and activity in part through reprograming of the cellular metabolism of major energy substrates. Recently, the lab has identified cell-intrinsic disruption of glucose metabolism as a pathogenic basis for osteoarthritis and diabetic osteopenia. In other projects, we combine single-cell sequencing technology with genetic lineage-tracing or functional studies to identify skeletal stem/progenitor cells in the mouse, and to examine their contribution to bone maintenance or pathology.
8
19 Rotation Projects
4c Metabolic and epigenetic reprogramming during cell differentiation
60 Functional dissection of metabolic pathways in the skeleton of genetically modified mice
41 Lineage tracing of skeletal stem/progenitor cells in vivo
29 Other projects open for discussion
e 29
27
Description of Research Expertise
23 Research Interests9d The Long lab seeks to understand the fundamental mechanisms underlying both normal skeletal development and the pathophysiology of bone disorders.
8
11 Key Words
c3 mesenchymal stem/progenitor cells, metabolic and epigenetic regulation, skeletal cell differentiation and function, diabetic osteopenia, skeletal aging, bone development and regeneration
8
18 Research Details
520 Skeletal diseases, ranging from congenital dysplasia to osteosarcoma to osteoarthritis and osteoporosis, take a significant toll on human health. The overarching goal of our research is to discover key steps in the molecular or metabolic regulation of skeletal cell differentiation or function, with the hope of uncovering therapeutic targets for treating the various skeletal diseases. Many of our studies have centered around the role and mechanism of key developmental signals such as Hh, Wnt, Notch and Bmp in regulating skeletal development and homeostasis. Through mouse genetic studies, we have defined specific functions of the developmental signals in bone and cartilage cell differentiation. Our molecular and biochemical studies have led to the discovery that the developmental signals alter cell fate and activity in part through reprograming of the cellular metabolism of major energy substrates. Recently, the lab has identified cell-intrinsic disruption of glucose metabolism as a pathogenic basis for osteoarthritis and diabetic osteopenia. In other projects, we combine single-cell sequencing technology with genetic lineage-tracing or functional studies to identify skeletal stem/progenitor cells in the mouse, and to examine their contribution to bone maintenance or pathology.
8
19 Rotation Projects
4c Metabolic and epigenetic reprogramming during cell differentiation
60 Functional dissection of metabolic pathways in the skeleton of genetically modified mice
41 Lineage tracing of skeletal stem/progenitor cells in vivo
29 Other projects open for discussion
e 29
23
13d Song C, Sawall JK, Ji X, Song F, Liao X, Peng R, Ren H, Koyama E, Pacifici M, Long F.: Tgfβ signaling stimulates glycolysis to promote the genesis of synovial joint interzone in developing mouse embryonic limbs. Sci Adv 11: eadq4991, Jan 2025.
b8 Bertels JC, He G, Long F.: Metabolic reprogramming in skeletal cell differentiation. Bone Res 12: 57, Oct 2024.
11f Song C, Valeri A, Song F, Ji X, Liao X, Marmo T, Seeley R, Rutter J, Long F.: Sexual dimorphism of osteoclast reliance on mitochondrial oxidation of energy substrates in the mouse. JCI Insight 8: e174293, Dec 2023.
120 Ji X, Seeley R, Li K, Song F, Liao X, Song C, Angelozzi M, Valeri A, Marmo T, Lee WC, Shi Y, Long F: Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes. Cell Chem Biol. July 2023.
10f Song F, Lee WD, Marmo T, Ji X, Song C, Liao X, Seeley R, Yao L, Liu H, Long F: Osteoblast-intrinsic defect in glucose metabolism impairs bone formation in type II diabetic male mice. Elife May 2023.
12f Li K, Ji X, Seeley R, Lee WC, Shi Y, Song F, Liao X, Song C, Huang X, Rux D, Cao J, Luo X, Anderson SM, Huang W, Long F: Impaired glucose metabolism underlies articular cartilage degeneration in osteoarthritis. FASEB J. June 2022.
d2 Lee WC, Ji X, Nissim I, Long F.: Malic Enzyme Couples Mitochondria with Aerobic Glycolysis in Osteoblasts. Cell Rep 32: 108108, Sep 2020.
f8 Seung-Yon Lee and Fanxin Long: Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. JCI 128(12): 5573, Dec. 2018.
de Lee SY, Abel ED, Long F: Glucose metabolism induced by Bmp signaling is essential for murine skeletal development. Nat Commun. 9(1): 4831, Nov. 2018.
2c
7
1d
1f
Selected Publications
145 Liao X, Koehnken Sawall J, Seeley R, Song F, Ji X, Liu X, Song C, Long F.: An adipo-osteoprogenitor population in the endosteal niche contributes to bone and fat formation in adult mouse bone marrow. Proc Natl Acad Sci U S A 122: e2502436122, Nov 2025.13d Song C, Sawall JK, Ji X, Song F, Liao X, Peng R, Ren H, Koyama E, Pacifici M, Long F.: Tgfβ signaling stimulates glycolysis to promote the genesis of synovial joint interzone in developing mouse embryonic limbs. Sci Adv 11: eadq4991, Jan 2025.
b8 Bertels JC, He G, Long F.: Metabolic reprogramming in skeletal cell differentiation. Bone Res 12: 57, Oct 2024.
11f Song C, Valeri A, Song F, Ji X, Liao X, Marmo T, Seeley R, Rutter J, Long F.: Sexual dimorphism of osteoclast reliance on mitochondrial oxidation of energy substrates in the mouse. JCI Insight 8: e174293, Dec 2023.
120 Ji X, Seeley R, Li K, Song F, Liao X, Song C, Angelozzi M, Valeri A, Marmo T, Lee WC, Shi Y, Long F: Genetic activation of glycolysis in osteoblasts preserves bone mass in type I diabetes. Cell Chem Biol. July 2023.
10f Song F, Lee WD, Marmo T, Ji X, Song C, Liao X, Seeley R, Yao L, Liu H, Long F: Osteoblast-intrinsic defect in glucose metabolism impairs bone formation in type II diabetic male mice. Elife May 2023.
12f Li K, Ji X, Seeley R, Lee WC, Shi Y, Song F, Liao X, Song C, Huang X, Rux D, Cao J, Luo X, Anderson SM, Huang W, Long F: Impaired glucose metabolism underlies articular cartilage degeneration in osteoarthritis. FASEB J. June 2022.
d2 Lee WC, Ji X, Nissim I, Long F.: Malic Enzyme Couples Mitochondria with Aerobic Glycolysis in Osteoblasts. Cell Rep 32: 108108, Sep 2020.
f8 Seung-Yon Lee and Fanxin Long: Notch signaling suppresses glucose metabolism in mesenchymal progenitors to restrict osteoblast differentiation. JCI 128(12): 5573, Dec. 2018.
de Lee SY, Abel ED, Long F: Glucose metabolism induced by Bmp signaling is essential for murine skeletal development. Nat Commun. 9(1): 4831, Nov. 2018.
2c
7
1e
18
18
6
9
b
26
b
22
10
cb
22
31
22
Contact us
4eInstitute for Diabetes, Obesity and Metabolism
3b
Smilow Center for Translational Research
37
3400 Civic Center Boulevard, 12th Floor
2a
Philadelphia, PA 19104
3a
Phone: 215-898-0198 | Fax 215-898-5408
31
12
Directions
120
18
37
e
54
10
© Trustees of the University of Pennsylvania
12