专家人才库数据----中国科学院上海巴斯德研究所

Principal investigator2016

Name:	Mengle SHAO	Gender:
Education:	2007.09-2013.01, Ph.D., Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, CAS 2003.09-2007.07, BS, Shanghai Jiao Tong University
Academic degree:	Ph.D.	Academic title:	Principal Investigator
Departments:	Microbiota and Metabolic Disease	Discipline:	Metabolic regulation
Phone:		E-mail:	mlshao@ips.ac.cn
Mailing Address:	Life Science Research Building, 320 Yueyang Road, Xuhui District, 200031

Curriculum vitae:
2021.07-present, Principle investigator, Institut Pasteur of Shanghai, CAS 2019.02-2021.06, Assistant instructor, University of Texas Southwestern Medical Center 2013.11-2019.01, Postdoctoral researcher, University of Texas Southwestern Medical Center 2013.02-2013.10, Postdoctoral researcher, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, CAS

Research direction:
The global prevalence of obesity places a growing number of individuals on the risk of developing chronic metabolic disease. However, effective therapeutics for the prevention and treatment of obesity are still very limited, which urges new discoveries of new therapeutic targets and strategies to combat against obesity and its comorbidities. One of the determinants of metabolic health in obesity is the mode by which metabolic organs (e.g. adipose tissue, liver, etc.) remodel in the setting of excessive caloric intake. Our labs focus on the investigation the key events of metabolic organ remodeling in multiple physiological and pathological settings. Our previous and ongoing projects employ state-of-the-art approaches including inducible genetic models, single-cell/nucleus technologies, multi-omics analysis, and advanced imaging systems to extensively explore the plasticity, complexity and heterogeneity of metabolic organs at cellular and molecular levels. We aim to elucidate how the key factors (such as nutrient status and host-microbial homeostasis) determine metabolic organs remodeling modes, with the hope of opening new pharmacological opportunities of utilizing these regulatory mechanisms to promote metabolic organ health and maintain metabolic health in obesity.

Research direction:

The global prevalence of obesity places a growing number of individuals on the risk of developing chronic metabolic disease. However, effective therapeutics for the prevention and treatment of obesity are still very limited, which urges new discoveries of new therapeutic targets and strategies to combat against obesity and its comorbidities.

One of the determinants of metabolic health in obesity is the mode by which metabolic organs (e.g. adipose tissue, liver, etc.) remodel in the setting of excessive caloric intake. Our labs focus on the investigation the key events of metabolic organ remodeling in multiple physiological and pathological settings. Our previous and ongoing projects employ state-of-the-art approaches including inducible genetic models, single-cell/nucleus technologies, multi-omics analysis, and advanced imaging systems to extensively explore the plasticity, complexity and heterogeneity of metabolic organs at cellular and molecular levels. We aim to elucidate how the key factors (such as nutrient status and host-microbial homeostasis) determine metabolic organs remodeling modes, with the hope of opening new pharmacological opportunities of utilizing these regulatory mechanisms to promote metabolic organ health and maintain metabolic health in obesity.

Research progress:
Selected Publications 1. Shao M, Hepler C, Zhang Q, Shan B, Vishvanath L, Henry GH, Strand DW, Gupta RK. Pathological HIF1 Signaling Drives Adipose Progenitor Dysfunction in Obesity. *Cell Stem Cell. 2021;28(4):685-701* (Cover story; commented by Cell Stem Cell) 2. Shan B, Shao M, Zhang Q, Hepler C, Paschoal VA, Barnes SD, Vishvanath L, An YA, Malladi VS, Strand DW, Gupta OT, Oh D, Gupta RK. Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity. **Nat Metab. 2020;2(11):1332-1349 ( Co-first author)*** (Highlighted by Nature Reviews Endocrinology) 3. Zhang Z, Shao M, Hepler C, Zi Z, Zhao S, An YA, Zhu Y, Ghaben AL, Wang M, Li N, Onodera T, Joffin N, Crewe C, Zhu Q, Vishvanath L, Kumar A, Xing C, Wang QA, Gautron L, Deng Y, Gordillo R, Kruglikov I, Kusminski CM, Gupta RK, Scherer PE. Dermal Adipose Tissue Has High Plasticity and Undergoes Reversible Dedifferentiation in Mice. J Clin Invest. 2019;129(12):5327-5342 (* Co-first author) 4. Shao M, Vishvanath L, Busbuso NC, Hepler C, Shan B, Sharma AX, Chen S, Yu X, An YA, Zhu Y, Holland WL, Gupta RK. De novo adipocyte differentiation from Pdgfr？+ preadipocytes protects against pathologic visceral adipose expansion in obesity. *Nat Commun. 2018;9:890* 5. Shao M, Hepler C, Vishvanath L, MacPherson KA, Busbuso NC, Gupta RK. Fetal development of subcutaneous white adipose tissue is dependent on Zfp423. *Mol Metab. 2017;6:111-124* 6. Shao M, Ishibashi J, Kusminski CM, Wang QA, Hepler C, Vishvanath L, MacPherson KA, Spurgin SB, Sun K, Holland WL, Seale P, Gupta RK. Zfp423 maintains white adipocyte identity through suppression of the beige cell thermogenic gene program. *Cell Metab. 2016;23:1167-1184* 7. Liu Y, Shao M, Wu Y, Yan C, Jiang S, Liu J, Dai J, Yang L, Li J, Jia W, Rui L, Liu Y. Role for the endoplasmic reticulum stress sensor IRE1？ in liver regenerative responses. **J Hepatol. 2015;62:590-598 ( Co-first author)*** 8. Shao M, Shan B, Liu Y, Deng Y, Yan C, Wu Y, Mao T, Qiu Y, Zhou Y, Jiang S, Jia W, Li J, Li J, Rui L, Yang L, Liu Y. Hepatic IRE1？ regulates fasting-induced metabolic adaptive programs through the XBP1s-PPAR signalling. *Nat Commun. 2014;5:3528* 9. Shen H, Shao M, Cho KW, Wang S, Chen Z, Sheng L, Wang T, Liu Y, Rui L. Herbal constituent sequoyitol improves hyperglycemia and glucose intolerance by targeting hepatocytes, adipocytes, and beta-cells. **AJP- Endo Metab. 2012;302:E932-940 ( Co-first author)*** 10. Mao T, Shao M, Qiu Y, Huang J, Zhang Y, Song B, Wang Q, Jiang L, Liu Y, Han JD, Cao P, Li J, Gao X, Rui L, Qi L, Li W, Liu Y. PKA phosphorylation couples hepatic inositol-requiring enzyme 1？ to glucagon signaling in glucose metabolism. **PNAS. 2011;108:15852-15857 ( Co-first author)***

Research progress:

Selected Publications

1. Shao M, Hepler C, Zhang Q, Shan B, Vishvanath L, Henry GH, Strand DW, Gupta RK. Pathological HIF1 Signaling Drives Adipose Progenitor Dysfunction in Obesity. Cell Stem Cell. 2021;28(4):685-701 (Cover story; commented by Cell Stem Cell)

2. Shan B*, Shao M*, Zhang Q, Hepler C, Paschoal VA, Barnes SD, Vishvanath L, An YA, Malladi VS, Strand DW, Gupta OT, Oh D, Gupta RK. Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity. Nat Metab. 2020;2(11):1332-1349 (* Co-first author) (Highlighted by Nature Reviews Endocrinology)

3. Zhang Z*, Shao M*, Hepler C, Zi Z, Zhao S, An YA, Zhu Y, Ghaben AL, Wang M, Li N, Onodera T, Joffin N, Crewe C, Zhu Q, Vishvanath L, Kumar A, Xing C, Wang QA, Gautron L, Deng Y, Gordillo R, Kruglikov I, Kusminski CM, Gupta RK, Scherer PE. Dermal Adipose Tissue Has High Plasticity and Undergoes Reversible Dedifferentiation in Mice. J Clin Invest. 2019;129(12):5327-5342 (* Co-first author)

4. Shao M, Vishvanath L, Busbuso NC, Hepler C, Shan B, Sharma AX, Chen S, Yu X, An YA, Zhu Y, Holland WL, Gupta RK. De novo adipocyte differentiation from Pdgfr？+ preadipocytes protects against pathologic visceral adipose expansion in obesity. Nat Commun. 2018;9:890

5. Shao M, Hepler C, Vishvanath L, MacPherson KA, Busbuso NC, Gupta RK. Fetal development of subcutaneous white adipose tissue is dependent on Zfp423. Mol Metab. 2017;6:111-124

6. Shao M, Ishibashi J, Kusminski CM, Wang QA, Hepler C, Vishvanath L, MacPherson KA, Spurgin SB, Sun K, Holland WL, Seale P, Gupta RK. Zfp423 maintains white adipocyte identity through suppression of the beige cell thermogenic gene program. Cell Metab. 2016;23:1167-1184

7. Liu Y*, Shao M*, Wu Y, Yan C, Jiang S, Liu J, Dai J, Yang L, Li J, Jia W, Rui L, Liu Y. Role for the endoplasmic reticulum stress sensor IRE1？ in liver regenerative responses. J Hepatol. 2015;62:590-598 (* Co-first author)

8. Shao M*, Shan B*, Liu Y, Deng Y, Yan C, Wu Y, Mao T, Qiu Y, Zhou Y, Jiang S, Jia W, Li J, Li J, Rui L, Yang L, Liu Y. Hepatic IRE1？ regulates fasting-induced metabolic adaptive programs through the XBP1s-PPAR signalling. Nat Commun. 2014;5:3528

9. Shen H*, Shao M*, Cho KW, Wang S, Chen Z, Sheng L, Wang T, Liu Y, Rui L. Herbal constituent sequoyitol improves hyperglycemia and glucose intolerance by targeting hepatocytes, adipocytes, and beta-cells. AJP- Endo Metab. 2012;302:E932-940 (* Co-first author)

10. Mao T*, Shao M*, Qiu Y, Huang J, Zhang Y, Song B, Wang Q, Jiang L, Liu Y, Han JD, Cao P, Li J, Gao X, Rui L, Qi L, Li W, Liu Y. PKA phosphorylation couples hepatic inositol-requiring enzyme 1？ to glucagon signaling in glucose metabolism. PNAS. 2011;108:15852-15857 (* Co-first author)

Laboratory members:
Positions available (Research Associate/Assistant, Postdoctoral Fellow or Ph. D. Candidates).