Contact

Location:
8403 Floyd Curl Dr., Office 292.2, MC 8257
STRF-South Texas Research Facility
San Antonio, Texas 78229-3900

Department

Molecular Medicine

Mengwei Zang, MD, PhD

Professor of Molecular Medicine
The Ewing Halsell Distinguished Chair in Research
Associate Director of the MD/PhD Program at UT Health San Antonio
Sam and Ann Barshop Institute for Longevity and Aging Studies

Education

YearDegreeDisciplineInstitution
1984MDMedicineWannan Medical College
Anhui Province , China
1987MSPathophysiologyHenan Medical University
Henan Province , China
1998PhDPharmacologyChinese Academy of Medical Sciences & Peking Union Medical College
Beijing , China
1999Postdoctoral FellowshipGastroenterology and PharmacologyMayo Clinic College of Medicine
Rochester , MN
2003Postdoctoral FellowshipDiabetes and Signal TransductionBoston University School of Medicine
Boston , MA

Research

Zang Laboratory Research

Dr. Mengwei Zang is an internationally recognized investigator in metabolism, diabetes, and age-related metabolic and liver diseases. Dr. Zang is a Professor of Molecular Medicine and the Ewing Halsell Distinguished Chair in Aging Research at the Barshop Aging Institute at the University of Texas Health San Antonio. Dr. Zang is also the Associate Director of the NIH-funded MSTP (MD/PhD) Program at the University of Texas Health San Antonio.

Dr. Zang’s laboratory focuses on the nutrient, transcriptional, or alternative splicing regulation of glucose and lipid metabolism. Her laboratory’s research is also aimed at identifying new therapeutic strategies and their underlying mechanisms for diabetes, chronic liver disease, and age-related metabolic and liver diseases. Despite significant research efforts to understand aging hallmarks, we are still unable to confidently answer fundamental questions: Why do we age? Can we delay the onset of age-related disease in humans? Using a variety of approaches, including genetically engineered mice, molecular biology, metabolomic and lipidomic analyses, and pharmacological approaches, the Zang Laboratory has discovered novel nutrient sensors and their specific pathways or networks that control metabolic homeostasis and defined how these processes are dysregulated in diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD), alcohol-associated liver disease (ALD), and aging-related metabolic and liver diseases. In particular, Dr. Zang’s laboratory has pioneered in deciphering the cellular and molecular mechanisms underlying nutrient sensors, such as an NAD+-dependent deacetylase SIRT1 or the hepatocyte-secreted hormone fibroblast growth factor 21 (FGF21), as well as in defining their impact on metabolic and liver disorders during aging. Key findings have been published in high-impact journals (Li Y, et al. Cell Metabolism, 2011; Gastroenterology, 2014; Luo T, et al. Diabetes, 2016, Chen H, et al, Hepatology, 2018, Li G, et al, Hepatology, 2023, Adjei-Mosi J, Aging Cell, 2023). Through collaborations with pharmaceutic companies, including Eli Lily and company as well as the Institute de Recherche Servier, these studies are serving as a platform for developing new therapeutics for treating diabetes and MASLD/MASH in humans. For instance, FGF21 is currently in Phase II clinical trials for the treatment of diabetes.

The long-term goal of the research in the Zang Laboratory is to translate these fundamental findings in cellular metabolism into potential therapeutic strategies for human metabolic diseases including the elderly population. Current research in Dr. Zang’s laboratory is focused on investigating the molecular mechanisms underlying the pathogenesis of MASLD/MASH and ALD associated with aging. The research goals of her lab are:

To investigate the role of nutrient sensing in controlling adipose tissue metabolism and dysfunction in obesity and diabetes—Zang lab’s studies have demonstrated that integration of AMPK activation and TGF-β1/Smad3 inhibition by metformin may provide a potential therapeutic approach to maintain ECM flexibility and combat chronically uncontrolled adipose tissue expansion and fibrosis in obesity.

To define the molecular mechanisms underlying the pathogenesis of alcohol-associated organ damage—Current efforts are primarily focused on the role of the mTORC1 pathway and its signaling network in the alcohol-induced lipogenesis and liver jury. Recent studies have indicated that hepatic DEPTOR-dependent inhibition of mTORC1 provides a potential druggable target for treating alcohol-associated liver disease in mice and humans.

To determine how the alternative splicing process contributes to the progression of chronic liver disease—Ongoing research is primarily focused on the regulation of alternative splicing machinery by the serine-arginine protein kinase 2 (SRPK2) and its impact on alcohol-associated liver disease.

To characterize the role of nutrient sensing in healthy aging and age-related liver disease—Current efforts are focused on the role of hepatocyte-derived signaling, such as SIRT1, in controlling age-related liver diseases such as liver fibrosis. Recent studies indicate that, unlike young mice, the age-dependent defect of SIRT1 in hepatocytes results in the activation of NLRP3 inflammasome and its associated inflammation. This process amplifies the initial insult and creates a vicious circle that impairs the capability to resolve fibrosis in old mice even after injury cessation. NLRP3 inhibition by the small molecule inhibitor, MCC950, ameliorates age- and alcohol-induced liver fibrosis. This inhibition effectively reduces inflammatory cell infiltration and suppresses hepatocyte-derived danger signaling through a feed-forward mechanism.

Lab Members


Seeking Postdoctoral Fellows in Cell Metabolism, Diabetes & Fatty Liver Disease

Department: Molecular Medicine

Where: Laboratory of Mengwei Zang, MD, PhD. Barshop Institute for Longevity and Aging Studies/Department of Molecular Medicine STRF-South Texas Research Facility University of Texas Health Science Center at San Antonio – San Antonio, TX

Nature of Work: Two POST-DOCTORAL FELLOWS in Diabetes and Fatty Liver Disease Two postdoctoral positions are available at Barshop Aging Institute of University of Texas Health Science Center at San Antonio, a leading institute in aging research, to work in the areas of signal transduction, cell metabolism, obesity, diabetes, fatty liver disease, and aging. Our ongoing research focuses on the nutrient regulation of glucose/lipid metabolism and energy balance, as well as the identification of new therapeutic mechanisms for fatty liver disease, diabetes and aging-related metabolic disease published in high impact journals (Li Y, et al. Cell Metabolism, 2011; Gastroenterology, 2014; Luo T, et al. Diabetes, 2016, Chen H, et al, Hepatology, 2018). We generate a variety of genetically modified mouse models and human disease-related animal models including obesity, diabetes, non-alcoholic fatty liver disease, and aging-related metabolic diseases. The ideal candidate are exceptionally motivated, creative, and committed to scientific discovery and have strong academic training in biochemistry, molecular and cell biology, and animal models. For more information of the research work of Zang laboratory, please visit https://directory.uthscsa.edu/academics/profile/zang; https://www.uthscsa.edu/academics/biomedical-sciences/profile/zang

Position Requirements: Candidates with a strong background in metabolism, ER stress or autophagy biology are strongly encouraged to apply for the positions. How to Apply: To apply, please submit a cover letter to Dr. Mengwei Zang at zang@uthscsa.edu and attach: curriculum vitae, a one-page personal statement describing your scientific accomplishments and research interests, and contact information (including phone numbers) of three references.

Contact Name: Mengwei Zang

Contact Email: zang@uthscsa.edu

Job Number: 118 All postdoctoral appointments are designated as security sensitive positions. UT Health San Antonio is an Equal Employment Opportunity/Affirmative Action employer including protected veterans and persons with disabilities.

News

Barshop Institute team discovers why liver disease is more severe in older people

Lower levels of a protective protein lead to liver inflammation, scarring

Contact: Will Sansom, 210-567-2579, sansom@uthscsa.edu

SAN ANTONIO (Oct. 3, 2023) ­— Researchers at The University of Texas Health Science Center at San Antonio (also called UT Health San Antonio) have identified a molecular pathway that connects aging to end-stage liver disease. A set of mechanistic processes, observed in mice fed an ethanol diet to mimic alcohol-related liver injury, offers clues for why older people suffer more serious and persistent liver damage than younger people do, even after liver injury is stopped.

The laboratory of Mengwei Zang, MD, PhD, at the health science center’s Sam and Ann Barshop Institute for Longevity and Aging Studies, reported the findings earlier this year in Aging Cell.

“Why are older individuals more likely to develop chronic liver disease compared to the young?” said Zang, professor of molecular medicine and the Ewing Halsell Distinguished Chair in Research at UT Health San Antonio. “What goes wrong with the aging liver that increases the risk of liver disease? Can we reverse these processes and maintain a younger, healthier liver? We seek answers to these questions.” Zang is also associate director of the South Texas Medical Scientist Training Program, which is the National Institutes of Health-funded MD-PhD dual-degree program at the health science center.

Liver fibrosis (or scarring) progresses in affected individuals during aging, and the cause was a mystery, Zang said. No approved treatment is available for this condition, even as the United Nations projects that the global population of people over the age of 65 will reach 1.5 billion by 2050. “A growing concern is the rising prevalence of complex chronic diseases, such as liver fibrosis, among older adults,” Zang said. “Tackling age-onset liver diseases is becoming an urgent public health and economic challenge.”

A team that included graduate students in UT Health San Antonio’s Personalized Molecular Medicine Program conducted the study. Students Jennifer Adjei-Mosi, Steven Blake Smithson and Gavyn Shealy, and a postdoctoral fellow in the lab, Qing Sun, MD, PhD, shed light on the link between SIRT1, a protein that promotes longevity but declines dramatically with aging, and NLRP3, a protein that regulates inflammation.

The research team includes the Aging Cell paper’s first author, Jennifer Adjei-Mosi, right, a Personalized Molecular Medicine (PMM) Program student who graduated from UT Health San Antonio in May 2022; Steven Blake Smithson, left, PMM student (Class of 2021); Gavyn Lee Shealy, center, PMM student (Class of 2022); and Mengwei Zang, MD, PhD, in blue and black academic regalia.

“Age-related loss of SIRT1 in the liver accelerated the progression of liver fibrosis by promoting NLRP3-mediated inflammation and by increasing hepatic stellate cells, a liver cell type responsible for producing collagen proteins that contribute to formation of scarring,” Zang said.

Young mice were observed to reverse liver fibrosis after injury cessation. Over time, hepatic stellate cell activation lowered, likely due to the restoration of hepatic SIRT1, which corralled NLRP3 activity.

In older mice, a severe form of liver fibrosis continued even after the injury ceased. “It was difficult to resolve the fibrosis that had developed,” Zang said. In these mice, as in older humans and animals, hepatic SIRT1 levels were very low.

Hepatic stellate cells are calm in the normal liver, but they secrete collagen when activated. The effect is a very stiff and thick scaffold of scar tissue called extracellular matrix. Collagen is one part of this matrix.

To test the hypothesis that diminished hepatic SIRT1 in old mice results in NLRP3-induced inflammation and scar formation, the Zang lab tested a known NLRP3 inhibitor called MCC950. In older mice given MCC950, alcohol-induced fibrosis resolved as NLRP3 signaling decreased, reducing inflammation, and stellate cell activation lessened, halting collagen deposition.

“Interventions such as NLRP3 inhibitors could help to keep the liver younger and healthier, reducing liver inflammation and slowing the progression of age-related liver fibrosis,” Zang said.

Most preclinical studies aimed at understanding liver fibrosis are performed in young mice, she said. Zang suggested that researchers could use older mice in developing drug therapies for liver fibrosis associated with aging, because her laboratory findings indicate that the ability of older livers to resolve liver fibrosis may be diminished compared to young livers.

Age-dependent loss of hepatic SIRT1 enhances NLRP3 inflammasome signaling and impairs capacity for liver fibrosis resolution

Jennifer Adjei-Mosi, Qing Sun, Steven Blake Smithson, Gavyn Lee Shealy, Krupa Dhruvitha Amerineni, Zerong Liang, Hanqing Chen, Mei Wang, Qinggong Ping, Jingyan Han, Masahiro Morita, Amrita Kamat, Nicolas Musi and Mengwei Zang

First published: March 31, 2023, Aging Cell

https://onlinelibrary.wiley.com/doi/10.1111/acel.13811


Study links alcohol-associated liver disease to abnormal cutting and rejoining of molecules

Splicing deregulation is potential drug target and diagnostic tool

Contact: Will Sansom, 210-567-2579, sansom@uthscsa.edu

SAN ANTONIO (July 25, 2023) — Alcohol consumption is a major cause of chronic liver disease. The disease, which has devastating consequences, progresses through stages of hepatitis (inflammation), fibrosis (scarring) and cirrhosis (severe scarring). Advanced disease increases the risk of developing liver cancer, and some individuals may require a liver transplant to live.

Despite a tremendous need for new treatments, the specific biological factors that determine when and how rapidly liver cells deteriorate remain largely unknown.

In a study published May 3 in the journal Hepatology, a research team at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) shines light on the disease process, including a possible therapeutic approach for combating alcohol-associated liver disease.

Mengwei Zang, MD, PhD

The researchers include Mengwei Zang, MD, PhD, the study’s senior author, who is professor of molecular medicine and the Ewing Halsell Distinguished Chair in Research within the health science center’s Sam and Ann Barshop Institute for Longevity and Aging Studies. She also serves as associate director of the National Institutes of Health-designated South Texas Medical Scientist Training Program at UT Health San Antonio. This program offers a cohesive dual-degree MD/PhD training experience to outstanding students.

“In our study, we show that the cutting and rejoining of molecules called pre-messenger RNAs is associated with liver disease caused by excessive alcohol consumption,” Zang said.

“We observed this link in both mice and humans, shedding light on the biological role of pre-mRNA splicing in maintaining steady liver metabolic function,” Zang said. “Moreover, our findings suggest that targeting specific splicing factors in liver cells called hepatocytes could offer a novel approach to mitigate alcohol-associated liver disease.”

It’s been known that certain splicing defects can lead to cancer cell processes, but the UT Health San Antonio team was intrigued about the role of abnormal pre-mRNA splicing in driving alcohol-related liver disease since practically nothing is known about the latter, Zang said.

One of Zang lab’s findings hints that splicing activity could help predict liver fat accumulation in individuals even before advanced disease such as fibrosis is apparent.

“This is a highly interesting result and suggests that splicing deregulation could potentially be used as an early indicator of fatty liver disease,” Zang said.

In mouse studies, the UT Health San Antonio team studied FGF21, a protein secreted by liver cells. FGF21 eased the alcohol-associated liver disease, possibly by inhibiting a splicing protein called SRPK2.

“Targeting SRPK2 signaling by FGF21 may represent a potential therapeutic approach for combating alcohol-associated liver disease,” Zang said.

Acknowledgments

This work was supported in part by the National Institutes of Health (grants RO1 DK100603, RO1 DK121527, and R21 AA026922 to Mengwei Zang, PhD). Zang is also supported in part by the Distinguished Chair Endowment Fund in Research from the Ewing Halsell Foundation at The University of Texas Health Science San Antonio.

Targeting hepatic serine-arginine protein kinase 2 ameliorates alcohol-associated liver disease by alternative splicing control of lipogenesis

Guannan Li, Hanqing Chen, Feng Shen, Steven Blake Smithson, Gavyn Lee Shealy, Qinggong Ping, Zerong Liang, Jingyan Han, Andrew C. Adams, Yu Li, Dechun Feng, Bin Gao, Masahiro Morita, Xianlin Han, Tim H Huang, Nicolas Musi and Mengwei Zang

First published: Hepatology, May 3, 2023

https://journals.lww.com/hep/Abstract/9900/Targeting_hepatic_serine_arginine_protein_kinase_2.418.aspx


Dr. Zang received R01 and R21 research grants from the NIH in June 2019.


Naturally occurring protein could treat alcoholic liver disease
Published On: June 25, 2018 Shared by Will Sansom


Mengwei Zang, MD, PhD, of UT Health San Antonio, with fellow researchers Hanqing Chen, PhD, center, and Feng Shen, MD, PhD

Chronic alcohol drinking affects 16 million people in the United States, and one of the results is fatty liver damage leading to cirrhosis (scarring). Liver cirrhosis is the 12th-leading cause of death nationwide. Researchers at UT Health San Antonio’s Sam & Ann Barshop Institute for Longevity & Aging Studies and Department of Molecular Medicine have identified a nutrient-sensing pathway that, if it can be blocked by pharmacological means, could either prevent this liver damage or be a treatment for it. The scientists believed chronic alcohol consumption would increase activity of a nutrient sensor called mTORC1 and that this would play a role in alcoholic fatty liver, said Mengwei Zang, MD, PhD, associate professor of molecular medicine at UT Health San Antonio. Dr. Zang, the Ewing Halsell Distinguished Chair at the university, is the senior author of alcohol liver disease research published this year in the journal Hepatology. To find out, the researchers measured liver mTORC1 levels in two groups of mice. Both groups drank a normal liquid diet for five days, with one group continuing on the normal diet for the duration of the study. The other group received a 5 percent ethanol liquid diet for 10 days and was allowed a one-time binging of the ethanol diet on day 16. “We found exciting results—chronic alcohol consumption increased liver mTORC1 activity in mice and in patients,” Dr. Zang said.

Normal liver (mouse)
Alcoholic fatty liver

Dr. Zang also reported that a protein called DEPTOR inhibits mTORC1 activity. Because DEPTOR is a naturally occurring protein in our bodies, she views it as a promising target of intervention to curb the fatty liver disease process. Rapamycin is a compound that reduces mTORC1 activity. The UT Health San Antonio team, including first author Hanqing Chen, PhD, and second author Feng Shen, MD, PhD, conducted further studies in which they compared two groups of mice that were fed an ethanol liquid diet. One group additionally received rapamycin while the other did not. The rapamycin treatment group showed inhibited mTORC1 activity and decreased liver damage, Dr. Zang said. “Based on these interesting findings, I hope in the future that we can target DEPTOR, perhaps with a pill, and treat alcoholic fatty liver disease,” she said.

Publications

Targeting Hepatic Serine-Arginine Protein Kinase 2 Ameliorates Alcohol-Associated Liver Disease by Alternative Splicing Control of Lipogenesis.
Li G, Chen H, Shen F, Smithson SB, Shealy G, Ping Q, Liang Z, Han J, Adams AC, Feng D, Gao B, Morita M, Han X, Huang TH, Musi N, Zang M.
Hepatology, 2023 May 3. doi: 10.1097/HEP.0000000000000433. Online ahead of print.
Age-dependent Loss of Hepatic SIRT1 Enhances NLRP3 Inflammasome Signaling and Impairs Capacity for Liver Fibrosis Resolution.
Adjei-Mosi J, Sun Q, Smithson SB, Shealy GL, Amerineni KD, Liang Z, Chen H, Wang M, Ping Q, Han J, Morita M, Kamat A, Musi N, Zang M.
Aging Cell. 2023 Mar 31; e13811.doi: 10.1111/acel.13811. PMID: 36999514.
SIRT6: therapeutic target for nonalcoholic fatty liver disease.
Zang M, Gao B.
Trends Endocrinol Metab. 2022, 33 (12): 801-803. doi: 10.1016/j.tem.2022.10.004. PMCID: PMC9757836
Distinct histopathological phenotypes of severe alcoholic hepatitis suggest different mechanisms driving liver injury and failure.
Ma J, Guillot A, Yang Z, Mackowiak B, Hwang S, Park O, Peiffer BJ, Ahmadi AR, Melo L, Kusumanchi P, Huda N, Saxena R, He Y,1 Guan Y, Feng D, Sancho-Bru P, Zang M, Cameron AM, Bataller R, Tacke F, Sun Z, Liangpunsakul S, Gao B.
J Clin Invest. 2022;132(14): e157780. doi: 10.1172/JCI157780. PMCID: PMC9282929.
LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance.
He S, Ryu J, Liu J, Luo H, Lv Y, Langlais P, Wen J, D Feng, Sun Z, Xia W, Lynch J, Druggirala R, Nicolson B, Zang M, Shi Y, Zhang F, Liu F, Juli Bai, Lily Dong.
J Clin Invest. 2021; 131(24): e148545. doi: 10.1172/JCI148545. PMCID: PMC8670837.
Alcohol binge drinking selectively stimulates protein S-glutathionylation in the aorta and liver of ApoE−/− mice.
Seidel K, Wan X, Zhang M, Zhou Y, Zang M, Han J.
Front Cardiovasc Med. 2021; 8:649813. doi: 10.3389/fcvm. PMCID: PMC8007763.
β2-Adrenergic receptor agonist induces hepatic steatosis in mice: Modeling nonalcoholic fatty liver disease in hyperadrenergic state.
Shi Y, Pizzini J, Hanzhou Wang H, Das F, Azees PA, Choudhury GG, Barnes J, Zang M, Weintraub ST, Yeh CK, Katz M, Kamat A.
American Journal of Physiology-Endocrinology and Metabolism. 2021;321(1): E90-E104. PMID: 34029162.
Hepatic posttranscriptional network comprised of CCR4-NOT deadenylase and FGF21 maintains systemic metabolic homeostasis.
Morita M, Siddiqui N, Katsumura S, Rouya C, Larsson O, Nagashima T, Hekmatnejad B, Takahashi A, Kiyonari H, Zang M, St-Arnaud R, Oike Y, Giguère V, Topisirovic I, Okada-Hatakeyama M, Yamamoto T, Sonenberg N.
Proc Natl Acad Sci U S A. 2019 Apr 16;116(16):7973-7981. doi: 10.1073/pnas.1816023116. Epub 2019 Mar 29. PMID: 30926667; PMCID: PMC6475422.
DEP domain-containing mTOR-interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute-on-chronic liver injury in alcoholic liver disease.
Chen H, Shen F, Sherban A, Nocon A, Li Y, Wang H, Xu MJ, Rui X, Han J, Jiang B, Lee D, Li N, Keyhani-Nejad F, Fan JG, Liu F, Kamat A, Musi N, Guarente L, Pacher P, Gao B, Zang M.
Hepatology. 2018 Aug;68(2):496-514. doi: 10.1002/hep.29849. Epub 2018 May 21. PMID: 29457836; PMCID: PMC6097912.
Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating sirtuin 1 expression.
Ramirez T, Li YM, Yin S, Xu MJ, Feng D, Zhou Z, Zang M, Mukhopadhyay P, Varga ZV, Pacher P, Gao B, Wang H.
J Hepatol. 2017 Mar;66(3):601-609. doi: 10.1016/j.jhep.2016.11.004. Epub 2016 Nov 18. PMID: 27871879; PMCID: PMC5316497.
AMPK Activation by Metformin Suppresses Abnormal Extracellular Matrix Remodeling in Adipose Tissue and Ameliorates Insulin Resistance in Obesity.
Luo T, Nocon A, Fry J, Sherban A, Rui X, Jiang B, Xu XJ, Han J, Yan Y, Yang Q, Li Q, Zang M.
Diabetes. 2016 Aug;65(8):2295-310. doi: 10.2337/db15-1122. Epub 2016 May 13. PMID: 27207538; PMCID: PMC4955985.
The redox mechanism for vascular barrier dysfunction associated with metabolic disorders: Glutathionylation of Rac1 in endothelial cells.
Han J, Weisbrod RM, Shao D, Watanabe Y, Yin X, Bachschmid MM, Seta F, Janssen-Heininger YMW, Matsui R, Zang M, Hamburg NM, Cohen RA.
Redox Biol. 2016 Oct;9:306-319. doi: 10.1016/j.redox.2016.09.003. Epub 2016 Sep 11. PMID: 27693992; PMCID: PMC5045950.
Fibroblast growth factor 21 improves hepatic insulin sensitivity by inhibiting mammalian target of rapamycin complex 1 in mice.
Gong Q, Hu Z, Zhang F, Cui A, Chen X, Jiang H, Gao J, Chen X, Han Y, Liang Q, Ye D, Shi L, Chin YE, Wang Y, Xiao H, Guo F, Liu Y, Zang M, Xu A, Li Y.
Hepatology. 2016 Aug;64(2):425-38. doi: 10.1002/hep.28523. Epub 2016 Apr 15. PMID: 26926384; PMCID: PMC5726522.
Hepatic SIRT1 attenuates hepatic steatosis and controls energy balance in mice by inducing fibroblast growth factor 21.
Li Y, Wong K, Giles A, Jiang J, Lee JW, Adams AC, Kharitonenkov A, Yang Q, Gao B, Guarente L, Zang M.
Gastroenterology. 2014 Feb;146(2):539-49.e7. doi: 10.1053/j.gastro.2013.10.059. Epub 2013 Nov 1. PMID: 24184811; PMCID: PMC4228483.
Retinoic acid receptor β stimulates hepatic induction of fibroblast growth factor 21 to promote fatty acid oxidation and control whole-body energy homeostasis in mice.
Li Y, Wong K, Walsh K, Gao B, Zang M.
J Biol Chem. 2013 Apr 12;288(15):10490-504. doi: 10.1074/jbc.M112.429852. Epub 2013 Feb 19. PMID: 23430257; PMCID: PMC3624431.
AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin-resistant mice.
Li Y, Xu S, Mihaylova MM, Zheng B, Hou X, Jiang B, Park O, Luo Z, Lefai E, Shyy JY, Gao B, Wierzbicki M, Verbeuren TJ, Shaw RJ, Cohen RA, Zang M.
Cell Metab. 2011 Apr 6;13(4):376-388. doi: 10.1016/j.cmet.2011.03.009. PMID: 21459323; PMCID: PMC3086578.
Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver.
Li Y, Xu S, Giles A, Nakamura K, Lee JW, Hou X, Donmez G, Li J, Luo Z, Walsh K, Guarente L, Zang M.
FASEB J. 2011 May;25(5):1664-79. doi: 10.1096/fj.10-173492. Epub 2011 Feb 14. PMID: 21321189; PMCID: PMC3079300.
SIRT1 regulates hepatocyte lipid metabolism through activating AMP-activated protein kinase.
Hou X, Xu S, Maitland-Toolan KA, Sato K, Jiang B, Ido Y, Lan F, Walsh K, Wierzbicki M, Verbeuren TJ, Cohen RA, Zang M.
J Biol Chem. 2008 Jul 18;283(29):20015-26. doi: 10.1074/jbc.M802187200. Epub 2008 May 14. PMID: 18482975; PMCID: PMC2459285.