In one paragraphArticle in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
13 authors.
Ting WangDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.ORCID http://orcid.org/0000-0003-4318-8042 Aoxing ChengState Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230027, China.ORCID http://orcid.org/0000-0001-9143-2199 Lingyu KongState Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Weiyi YouState Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Jihua LiuState Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Xing LiuMinistry of Education Key Laboratory for Membraneless Organelles and Cellular Dynamics, University of Science and Technology of China, Hefei, Anhui, 230027, China.ORCID http://orcid.org/0000-0002-7480-5085 Xuebiao YaoMinistry of Education Key Laboratory for Membraneless Organelles and Cellular Dynamics, University of Science and Technology of China, Hefei, Anhui, 230027, China.ORCID http://orcid.org/0000-0001-8982-5911 Yi YangOptogenetics & Synthetic Biology Interdisciplinary Research Center, State Key Laboratory of Bioreactor Engineering, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, 200237, China.
Yuzheng ZhaoOptogenetics & Synthetic Biology Interdisciplinary Research Center, State Key Laboratory of Bioreactor Engineering, Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, 200237, China.ORCID http://orcid.org/0000-0001-5400-0135 Weiwei YangKey Laboratory of Multi-cell Systems, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. wyang@sibcb.ac.cn.ORCID http://orcid.org/0000-0002-1661-9137 Kaiguang ZhangDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China. zhangkaiguang@ustc.edu.cn.ORCID http://orcid.org/0000-0001-9462-6335 Zhenye YangDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China. zhenye@ustc.edu.cn.ORCID http://orcid.org/0000-0001-7797-5891 Jing GuoDepartment of Digestive Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China. jguo2013@ustc.edu.cn.ORCID http://orcid.org/0000-0002-0470-5417 Funding
MOST | National Key Research and Development Program of China (NKPs) 2022YFA1303100MOST | National Natural Science Foundation of China (NSFC) 32170736MOST | National Natural Science Foundation of China (NSFC) 32370776MOST | National Natural Science Foundation of China (NSFC) 92357301National Natural Science Foundation of China-Anhui joint found U25A20651National Science and Technology Major Project () 2023ZD0507500Research Funds of Center for Advanced Interdisciplinary Science and Biomedicine of IHM of USTC QYPY20220017The strategic priority research program of the Chinese academy of science XDB0940101
6 · The paper itselfAbstract
As cells progress from interphase into mitosis, fluctuating metabolic demands coincide with mitochondrial fission. However, the mechanisms by which mitochondria coordinate morphological changes and metabolic adjustments during mitosis remain poorly understood. Using proteomic analysis of BN-PAGE fractions, we show that assembly of the mitochondrial respiratory supercomplexes, comprising electron transport chain complexes I, III, and IV, is markedly enhanced during mitosis in HeLa and MDA-MB-468 cancer cells. Mechanistically, the upregulation of specific CI subunits, including NDUFA3, drives the modular assembly of supercomplexes in mitosis. We further demonstrate that CDK1 promotes the translation of NDUFA3 to enable supercomplex formation. Disruption of this process impairs mitochondrial integrity, energy production, and redox homeostasis, leading to ROS accumulation that triggers mitotic cell death and chromosome segregation defects across multiple models. Importantly, inhibiting mitotic supercomplex assembly induces chromosome mis‑segregation and suppresses tumor growth in vivo. Our findings reveal supercomplex assembly as a key mechanism coordinating mitochondrial fission with metabolic adaptation to support cell division and tumor proliferation in these cancer cell contexts.
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