Rencheng Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Rencheng Wang has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Che-Pei Kung
Department of Medicine, Division of Molecular Oncology, Washington University School of Medicine, Saint Louis, MO, USA
1 shared publication - Cong-Hui Yao
Department of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA
1 shared publication - Gary J. Patti
Department of Chemistry, Washington University in St. Louis, St. Louis, USA
1 shared publication Jason D Weber
Division of Molecular Oncology, Washington University School of Medicine, St. Louis, United States
1 shared publication- Yahui Wang
Department of Chemistry, Washington University, St. Louis, United States
1 shared publication
Latest Publications
- Top Cited PapersOpen Access
- 29 January 2019
- Published by eLife Sciences Publications, Ltd in eLife
- Vol. 8
Mitochondrial fusion supports increased oxidative phosphorylation during cell proliferation
Proliferating cells often have increased glucose consumption and lactate excretion relative to the same cells in the quiescent state, a phenomenon known as the Warburg effect. Despite an increase in glycolysis, however, here we show that non-transformed mouse fibroblasts also increase oxidative phosphorylation (OXPHOS) by nearly two-fold and mitochondrial coupling efficiency by ~30% during proliferation. Both increases are supported by mitochondrial fusion. Impairing mitochondrial fusion by knocking down mitofusion-2 (Mfn2) was sufficient to attenuate proliferation, while overexpressing Mfn2 increased proliferation. Interestingly, impairing mitochondrial fusion decreased OXPHOS but did not deplete ATP levels. Instead, inhibition caused cells to transition from excreting aspartate to consuming it. Transforming fibroblasts with the Ras oncogene induced mitochondrial biogenesis, which further elevated OXPHOS. Notably, transformed fibroblasts continued to have elongated mitochondria and their proliferation remained sensitive to inhibition of Mfn2. Our results suggest that cell proliferation requires increased OXPHOS as supported by mitochondrial fusion.
- 29 January 2019
- Published by eLife Sciences Publications, Ltd in eLife
- Vol. 8
Top Cited PapersOpen AccessMitochondrial fusion supports increased oxidative phosphorylation during cell proliferation
Proliferating cells often have increased glucose consumption and lactate excretion relative to the same cells in the quiescent state, a phenomenon known as the Warburg effect. Despite an increase in glycolysis, however, here we show that non-transformed mouse fibroblasts also increase oxidative phosphorylation (OXPHOS) by nearly two-fold and mitochondrial coupling efficiency by ~30% during proliferation. Both increases are supported by mitochondrial fusion. Impairing mitochondrial fusion by knocking down mitofusion-2 (Mfn2) was sufficient to attenuate proliferation, while overexpressing Mfn2 increased proliferation. Interestingly, impairing mitochondrial fusion decreased OXPHOS but did not deplete ATP levels. Instead, inhibition caused cells to transition from excreting aspartate to consuming it. Transforming fibroblasts with the Ras oncogene induced mitochondrial biogenesis, which further elevated OXPHOS. Notably, transformed fibroblasts continued to have elongated mitochondria and their proliferation remained sensitive to inhibition of Mfn2. Our results suggest that cell proliferation requires increased OXPHOS as supported by mitochondrial fusion.