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Kun Cheng

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Articles

B cells in cancer: functions, mechanisms and therapeutic advances

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By Hao Zhang, Kun Cheng, Ji Su Mo, Mingrui Chen, Ziran Zhou, Zhe Wang, Zheng Yang, Xiaoping Chen, Wanguang Zhang
| Nature Verified
Abstract Across various cancer entities, a wide array of subtypes of B cells that infiltrate tumors can be identified. These subtypes confer these cells with high adaptability in their functions and significant involvement in tumor progression. Tumor-infiltrating B cells act as distinctive microenvironmental mediators that build tertiary lymphoid structures, secrete diverse factors, and generate a wide antibody repertoire, thereby offering a valuable indicator of immunotherapy response.
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Vulnerability to high temperature shapes global warming impacts on rice yield

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By Guobin Yu, Ruoqi Liu, Yiwei Jian, Xuhui Wang, Jonas Jägermeyr, Philippe Ciais, Christoph Müller, Jakob Zscheischler, Tao Li, Kun Cheng, Pengfu Hou, Jianliang Huang, Shan Huang, Yu Jiang, Bin Wang, Zhenwei Song, Zuolin Zhang, Peng Zhu, Feng Zhou
| Science Magazine Verified
Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Complex and spatially varying warming impacts on rice yield hinder climate change impact assessments on food security. To address this issue, we compiled a global dataset of field-warming experiments (n = 214) and analyzed stage-specific crop responses to temperature variations.
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Mitochondrial Distress Signals at the Heart-Liver Interface: Molecular Links Between MASLD and Heart Failure

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By Xing Yang, Kun Cheng, Yuxin Zhang
| Preprints.org
You are already at the latest version Mitochondrial distress signaling provides a mechanistic link between local organelle dysfunction and systemic cardio-hepatic remodeling. In metabolic dysfunction-associated steatotic liver disease (MASLD) and heart failure (HF), hepatic nutrient overload and cardiac energy-demand mismatch generate distinct but convergent disturbances in oxidative metabolism, mitochondrial dynamics, mitophagy, and redox control.
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