Jonathan D. Holz

664 total citations
17 papers, 561 citations indexed

About

Jonathan D. Holz is a scholar working on Molecular Biology, Oncology and Rheumatology. According to data from OpenAlex, Jonathan D. Holz has authored 17 papers receiving a total of 561 indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Molecular Biology, 6 papers in Oncology and 5 papers in Rheumatology. Recurrent topics in Jonathan D. Holz's work include Bone Metabolism and Diseases (8 papers), Osteoarthritis Treatment and Mechanisms (4 papers) and Bone health and osteoporosis research (4 papers). Jonathan D. Holz is often cited by papers focused on Bone Metabolism and Diseases (8 papers), Osteoarthritis Treatment and Mechanisms (4 papers) and Bone health and osteoporosis research (4 papers). Jonathan D. Holz collaborates with scholars based in United States, China and Taiwan. Jonathan D. Holz's co-authors include Tzong‐Jen Sheu, J. Edward Puzas, Qi Shi, Quan Zhou, Eric E. Beier, Dezhi Tang, Tzong-Jen Sheu, Yongjun Wang, Minjie Zhang and Stephen E. Harris and has published in prestigious journals such as Journal of Biological Chemistry, PLoS ONE and Biochemical and Biophysical Research Communications.

In The Last Decade

Jonathan D. Holz

17 papers receiving 556 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Jonathan D. Holz United States 14 298 136 90 81 79 17 561
Soo Woong Lee South Korea 11 488 1.6× 63 0.5× 120 1.3× 205 2.5× 41 0.5× 18 738
Sylvie Sébillaud France 12 195 0.7× 111 0.8× 23 0.3× 27 0.3× 77 1.0× 26 475
Myeung Su Lee South Korea 16 539 1.8× 121 0.9× 96 1.1× 243 3.0× 12 0.2× 31 778
Birgit Mentrup Germany 18 326 1.1× 136 1.0× 86 1.0× 58 0.7× 206 2.6× 34 1.1k
Amy Carlos United States 7 310 1.0× 57 0.4× 199 2.2× 105 1.3× 17 0.2× 7 564
Niloufar Moradi‐Bidhendi United Kingdom 9 249 0.8× 76 0.6× 64 0.7× 91 1.1× 11 0.1× 11 650
Hao Lin China 12 422 1.4× 68 0.5× 42 0.5× 44 0.5× 10 0.1× 26 625
Gallic Beauchef France 13 154 0.5× 258 1.9× 42 0.5× 53 0.7× 15 0.2× 25 614
James B. Nold United States 10 337 1.1× 47 0.3× 270 3.0× 343 4.2× 36 0.5× 23 848
Yizhong Bao China 14 197 0.7× 242 1.8× 20 0.2× 32 0.4× 56 0.7× 37 605

Countries citing papers authored by Jonathan D. Holz

Since Specialization
Citations

This map shows the geographic impact of Jonathan D. Holz's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Jonathan D. Holz with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Jonathan D. Holz more than expected).

Fields of papers citing papers by Jonathan D. Holz

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Jonathan D. Holz. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Jonathan D. Holz. The network helps show where Jonathan D. Holz may publish in the future.

Co-authorship network of co-authors of Jonathan D. Holz

This figure shows the co-authorship network connecting the top 25 collaborators of Jonathan D. Holz. A scholar is included among the top collaborators of Jonathan D. Holz based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Jonathan D. Holz. Jonathan D. Holz is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

17 of 17 papers shown
1.
Lin, Liang‐Ting, Wen‐Chien Huang, Jonathan D. Holz, et al.. (2020). Up‐regulation of cofilin‐1 in cell senescence associates with morphological change and p27kip1‐mediated growth delay. Aging Cell. 20(1). e13288–e13288. 19 indexed citations
2.
Beier, Eric E., Jonathan D. Holz, Tzong‐Jen Sheu, & J. Edward Puzas. (2015). Elevated Lifetime Lead Exposure Impedes Osteoclast Activity and Produces an Increase in Bone Mass in Adolescent Mice. Toxicological Sciences. 149(2). 277–288. 28 indexed citations
3.
Beier, Eric E., Tzong‐Jen Sheu, Deborah Dang, et al.. (2015). Heavy Metal Ion Regulation of Gene Expression. Journal of Biological Chemistry. 290(29). 18216–18226. 30 indexed citations
4.
Wang, Meiqing, et al.. (2014). Activation of β-catenin signalling leads to temporomandibular joint defects. European Cells and Materials. 28. 223–235. 32 indexed citations
5.
Tang, Dezhi, Guohua Xu, Jonathan D. Holz, et al.. (2014). Biphasic calcium phosphate nano-composite scaffolds reinforced with bioglass provide a synthetic alternative to autografts in a canine tibiofibula defect model. Chinese Medical Journal. 127(7). 1334–1338. 3 indexed citations
6.
Wang, Jinwu, Xudong Wang, Jonathan D. Holz, et al.. (2013). Runx1 Is Critical for PTH-induced Onset of Mesenchymal Progenitor Cell Chondrogenic Differentiation. PLoS ONE. 8(9). e74255–e74255. 21 indexed citations
7.
Li, Xiaofeng, Hao Xu, Yongjian Zhao, et al.. (2013). Icariin Augments Bone Formation and Reverses the Phenotypes of Osteoprotegerin-Deficient Mice through the Activation of Wnt/β-Catenin-BMP Signaling. Evidence-based Complementary and Alternative Medicine. 2013. 1–13. 54 indexed citations
8.
Shi, Shanshan, Tianfang Li, Jonathan D. Holz, et al.. (2012). TIMP2 deficient mice develop accelerated osteoarthritis via promotion of angiogenesis upon destabilization of the medial meniscus. Biochemical and Biophysical Research Communications. 423(2). 366–372. 19 indexed citations
9.
Holz, Jonathan D., Eric E. Beier, Tzong‐Jen Sheu, et al.. (2012). Lead induces an osteoarthritis‐like phenotype in articular chondrocytes through disruption of TGF‐β signaling. Journal of Orthopaedic Research®. 30(11). 1760–1766. 15 indexed citations
10.
Holz, Jonathan D., et al.. (2011). Classic yin and yang tonic formula for osteopenia: study protocol for a randomized controlled trial. Trials. 12(1). 187–187. 12 indexed citations
11.
Tong, Peijian, Chengliang Wu, Hongting Jin, et al.. (2011). Gene Expression Profile of Steroid-induced Necrosis of Femoral Head of Rats. Calcified Tissue International. 89(4). 271–284. 21 indexed citations
12.
Hou, Wei, Quan Zhou, Minjie Zhang, et al.. (2010). Osthole stimulates osteoblast differentiation and bone formation by activation of β-catenin–BMP signaling. Journal of Bone and Mineral Research. 25(6). 1234–1245. 115 indexed citations
13.
Sheu, Tzong‐Jen, et al.. (2009). Putative signaling action of amelogenin utilizes the Wnt/β‐catenin pathway. Journal of Periodontal Research. 44(3). 289–296. 28 indexed citations
14.
15.
Zhou, Quan, Qianqian Liang, Jonathan D. Holz, et al.. (2008). IGF-1 regulation of type II collagen and MMP-13 expression in rat endplate chondrocytes via distinct signaling pathways. Osteoarthritis and Cartilage. 17(1). 100–106. 75 indexed citations
16.
Holz, Jonathan D., et al.. (2007). Environmental agents affect skeletal growth and development. Birth Defects Research Part C Embryo Today Reviews. 81(1). 41–50. 22 indexed citations
17.
Ryan, Elizabeth P., Jonathan D. Holz, Mary K. Mulcahey, et al.. (2007). Environmental Toxicants May Modulate Osteoblast Differentiation by a Mechanism Involving the Aryl Hydrocarbon Receptor. Journal of Bone and Mineral Research. 22(10). 1571–1580. 56 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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