· 1978-1982, 四川大學, 生物系, 主修生物化學, 學士學位

· 1990-1996,西奈山醫(yī)學院(The Mount Sinai School of Medicine, New York), 主修生物醫(yī)學科學（Biomedical Science）, 獲博士學位 ，Ph.D. 導師, Dr. Ronald A. Kohanski

· 1996-1999, 南加大洛杉磯兒童醫(yī)院Los Angeles Childrenu2019s Hospital/University of Southern California, 博士后 (1996-1999), 導師, Dr. Yun-Kai (Teddy) Fong

· 1982-1985, 地質(zhì)礦產(chǎn)部工藝研究所, 助理研究員

· 1985-1989, 四川抗菌素研究所, 助理研究員

· 1989-1990, SmithKline Pharmaceuticals (葛蘭素史克, 美國, 費城), 從事新藥發(fā)現(xiàn)研究

· 2000-2003, 南加州大學 University of Southern California, Keck School of Medicine, 助理研究員

· 2004-2011, 南加州大學 University of Southern California, Keck School of Medicine, 助理教授 (Assistant Professor at Tenure Track)。 USC Keck School of Medicine, PIBBS 博士研究生導師。

· 2004年-現(xiàn)在，南加州大學，Keck School of Medicine, 酒精肝病及胰腺疾病研究中心會員

· 2011-至今首都醫(yī)科大學，北京佑安醫(yī)院客座教授

· 2012-至今，Cedars-Sinai Medical Center (Los Angeles), 客座教授，項目合作。

· 2012-至今, 四川大學，生命科學學院，教授。

Journal of Clinical Investigation

Hepatology

American Journal of Pathology

American Journal of Physiology (Gastrointestinal and Liver Physiology)

Wound Repair and Regeneration Journal

Journal of Biological Chemistry

Life Science Journal

Journal of the National Cancer Institute

Journal of Cellular and Molecular Medicine

National Science Foundation (NSF)

Wellcome Foundation

National Institutes of Health (NIH)

中國自然基金

1. Principal Investigator: “ACT, a pathophysiological inhibitor of MMP-9 Activation”.

R01, AR051558, NIAMS, 7/1/2004-6/30/2009

The goal of this grant is to identify and characterize alpha-ACT as a novel inhibitor controlling proMMP9 conversion in human skin.

2. Principal Investigator: “Hepatic Stellate Cell Derived MMP9 in Liver Fibrogenesis”.

R01, DK069418, NIDDK, 9/1/2004-8/30/2009

The major goal of this grant is to elucidate the mechanism of fibrogenic activation of hepatic stellate cells, an essential process in liver fibrogenesis. Specifically, we have addressed the role of IL-1 in ECM remodeling and activation of hepatic stellate cells.

3. Pilot Project Investigator: “Cytokine regulation of MMPs and TIMPs by alcoholic liver”. 5P50AA011999, Pilot Project Grant, NIAAA, 12/30/2002-12/31/2004， The aims of this pilot project are to explore the roles of MMPs in hepatic stellate cell activation (trans-differentiation) and the inflammation mediated regulation of MMPs.

4. Principal Investigator: “Purification of the hepatic stellate cell produced proMMP-9 activator”

Robert E. and May R. Wright Foundation (II), 6/30/2004-6/30/2006 We recently demonstrated that IL-1a induced MMP-9 has an essential role in trans-differentiation of hepatic stellate cells. However, an outstanding question is that how proMMP-9 is converted into active form by hepatic stellate cells. This grant will support us to identify this activator through protein biochemical and genomic approaches. 5. Principal Investigator: “Identification of the Cellular Factors

Controlling MMP-9 Activation in Human Skin and Implication in Cancer Metastasis”. Robert E. and May R. Wright Foundation (I), 7/1/2002-6/30/2004

The aim of this project is to purify the putative proMMP-9 activator from human skin. Through the original work we have 1) defined the cytokine regulation of proMMP-9 activation by human skin, 2) established a protocol to extract the activator and 3) characterized the putative activator as a tissue bound chymotrypsin-like proteinase.

6. Principal Investigator: “The cellular factors promote MMP-9 activation in chronic wound". The Plastic Surgery Education Foundation, PI, 2000-2001 The aim of this grant is to understand the cytokine mediated induction of proMMP-9 expression by dermal fibroblasts and keratinocytes. The signal transduction leading expression MMP is the key emphasis.

7. Principal Investigator “Regulatory T cells in liver injury and fibrosis”.

Pilot Grant, NIDDK, issued by the Research Center of Liver Diseases. 3/15/2010-6/13/2011

8. 四川大學，海外人才引進計劃及985計劃，

啟動基金： ￥ 800,000

2012/9/1 u2013 2016/9/1

9.中國肝炎防治基金會王寶恩肝纖維化研究基金

“調(diào)節(jié)性T－細胞在重度肝纖維化及肝硬化中的關鍵作用”。

￥ 50,000，2014/5/1 － 2015/5/1.

10. 四川省科技支撐計劃項目

“脂肪性肝炎發(fā)生的系統(tǒng)生物學及抗脂肪肝的新療法”13002656942188

￥ 200,000；2014/11/13 － 2016/11/13

11. 成都通德制藥公司

“對通德制藥公司現(xiàn)有藥物的二次開發(fā)”

￥ 650,000；2014/11/20 － 2016/11/20

12. 中國自然基金

“維生素D調(diào)節(jié)腸道抗菌肽及菌群，以低于代謝綜合癥”。#31571165￥ 748,000：2016/01 － 2019/12.

(1) 代謝綜合癥，脂肪肝的機理及新療法的開發(fā)。

近年來我們將工作的重點的一部分轉(zhuǎn)移到代謝綜合癥，脂肪肝，肥胖的機理研究及新藥物的開發(fā)。隨著社會經(jīng)濟的巨大發(fā)展，代謝綜合癥（Metabolic Syndrome，MS) 表現(xiàn)為高血脂，脂肪肝，肥胖，糖尿病，呈蔓延之勢。近來官方的統(tǒng)計，中國有1億六千萬人群患有不同程度的代謝綜合癥。在西方，四分之一的成人為肥胖。代謝綜合癥的危險性在于引發(fā)糖尿病，心血管疾病，及腦中風，已成為最主要的死亡殺手。代謝綜合癥的發(fā)生與高糖，高脂肪飲食有密切關系。改善飲食及生活方式是治療代謝綜合癥的有效方法。在藥物治療方法，降膽固醇，降高血壓，降血糖是主要的策略。另外，使異位的脂肪（腹內(nèi)）回歸到脂肪皮下細胞，也是防治代謝綜合癥的新方向�；�于多年來我們在慢性疾病研究的經(jīng)驗，我們采用系統(tǒng)生物學的方法，從新的角度及方法來研究代謝綜合癥。代謝綜合癥的發(fā)生分為三個階段。第一步，高脂肪，高果糖飲食引起的腸道菌群(microbiota)的改變，造成血液內(nèi)毒素的上升及腹部脂肪組織的慢性炎癥。第二步，慢性炎癥造成胰島素抵抗，糖耐受，II型糖尿病。作為彌補機制，高血糖在肝臟轉(zhuǎn)化為脂肪酸，形成高血脂，脂肪肝。而脂肪肝及腹內(nèi)脂肪產(chǎn)生的炎癥會造成肝臟損傷，導致高密度脂蛋白（HDL）下降，凝血機制增強。第三步，持續(xù)的糖尿病，高血脂，凝血異常，將產(chǎn)生心血管阻塞，中風，加速死亡。為此，我們以系統(tǒng)生物學的方法，發(fā)現(xiàn)高脂肪飲食及維生素D缺乏誘導腸道菌群的改變，Paneth細胞抗菌多肽的下降，腸道及腹內(nèi)脂肪，胰腺的低度炎癥，造成胰島素抵抗，產(chǎn)生脂肪肝，糖耐受。以此模型， 我們將闡述代謝綜合癥的發(fā)生機理。同時，我們正在研究開發(fā)全新的藥物，用于代謝綜合癥的預防及治療。

（2）組織纖維化的細胞生物學。

在美國南加大（University of Southern California)工作期間，作為PI并在兩個NIH R01基金的資助下，我們長期從事這方面的研究。廣義的組織損傷包括病毒感染，污染毒物的攝入，及多種慢性疾病，腫瘤等等。損傷以后，肌體有兩種選擇，是再生，還是修復。大多數(shù)的組織僅有極小的再生能力（例如肝臟，皮膚）。而采用修復是大規(guī)�；蚴浅掷m(xù)損傷的首要選擇。修復的主要特征是產(chǎn)生纖維化的組織結(jié)構(gòu)。作為進化的選擇結(jié)果，組織纖維化對于肌體是有益的，它為失去的組織打上了“補丁”，否則因失去的組織，個體不能幸存。但是，持續(xù)的纖維化將使得慢性疾病，例如腫瘤得以持續(xù)。器官的老年衰竭也是組織纖維化的結(jié)果。據(jù)估計，大約50%的死亡都與組織纖維化有關。大多數(shù)的腫瘤之所以能夠持續(xù)的原因，在很大程度上是因為纖維化組織為腫瘤提供了生長的環(huán)境。我們的工作主要集中于肝星狀細胞(hepatic stellate cells) 的轉(zhuǎn)分化（trans-differentiation)。我們發(fā)現(xiàn)在肝星狀細胞轉(zhuǎn)分化過程中，多個MMP基因被不可逆地關閉，消靜（silencing）。我們認為，在正常肝血竇中星狀細胞的表型是有其3維ECM通過表觀遺傳（epigenetic control) 所決定的。更進一步，根據(jù)我們的發(fā)現(xiàn)，我們認為3D ECM通過下調(diào)II－型HDAC，使MMP基因群（mmp loci) 處于表觀遺傳水平的開放狀態(tài)，在炎癥因子引發(fā)的信號傳導下，能夠大量表達，釋放生長因子，開啟損傷及修復。星狀細胞在生長因子的促動下轉(zhuǎn)化為肌成纖維母細胞（myofibroblasts), 并形成纖維組織。MMP基因在肌成纖維母細胞的消靜，將促進ECM的積累以及纖維化。我們發(fā)現(xiàn)，在星狀細胞轉(zhuǎn)分化過程中，II－型HDAC趨于上升，蛋白質(zhì)穩(wěn)定，導致MMP基因被抑制。我們將繼續(xù)回答以下問題：（1）MMP基因群的表觀遺傳景觀在轉(zhuǎn)分化過程中的改變，從開放到抑制？（2）II－型HDAC的降解酶，以及在纖維化中的作用？（3）3D ECM對II－型HDAC的調(diào)控以及在損傷中MMP基因的表達。

（3）肝纖維化中的免疫耐受。

肝纖維化不但是由于星狀細胞的轉(zhuǎn)分化及肌纖維母細胞的形成，同樣重要的是肝硬化所處的免疫賴受的宏觀環(huán)境（macro-environment of immune tolerance），使得纖維組織免于被清除，逃逸免疫監(jiān)控 (escaping from immune surveillance)。同時，免疫賴受也為腫瘤生長，轉(zhuǎn)移，惡化提供環(huán)境條件。在前期工作中，我們發(fā)現(xiàn)天然調(diào)節(jié)性T細胞（naturally occurring Tregs, nTres) 在肝損傷中的下降是由于其細胞凋亡所致，而在肝修復過程中產(chǎn)生的誘導型Tregs（induced Tregs， iTregs）是由于MMP激活的TGF－beta從而誘道Foxp3所致。該工作近來被Journal of Molecular Cell Biology (影響因子: 7.3) 接受。我們發(fā)現(xiàn)伴隨肝纖維化的形成，Tregs聚集于纖維橋附近，說明Tregs產(chǎn)生的免疫賴受可能促進纖維化的持續(xù)。當我們用單抗干預Tregs時，發(fā)現(xiàn)能夠促進小鼠肝硬化的消融，表明Tregs可能抑制纖維的消融。我們發(fā)現(xiàn)Tregs通過上調(diào)TIMP來抑制MMP。同時，我們在肝硬化病人的肝組織中檢出Tregs的升高，說明可能的因果關系。為此，我們提出新的假設：肝星狀細胞所釋放的MMP通過激活TGF－beta，并且在IL－1作用下釋放維甲酸（retinoic acid）來誘導Tregs，使纖維化免于被清除。另一方面，與北京佑安醫(yī)院合作，我們也對II－型巨噬細胞（alternatively activated macrophages) 在纖維化的免疫耐受開展了大量工作。

Peer-Reviewed

1. Yuan-Ping Han, Kohanski RA.

“Phenylarsine oxide inhibits insulin activation of phosphatidylinositol 3’-kinase”.

Biochem Biophys Res Commun 1997 Oct 9;239 (1):316-21.

2. Frankel M, Bishop SM, Ablooglu AJ, Yuan-Ping Han, Kohanski RA. “Conformational changes in the activation loop of the insulin receptor’s kinase domain”.

Protein Science 1999 Oct; 8(10): 2158-65.

3. Yuan-Ping Han, Tuan TL, Wu H, Hughes M, Garner WL.

“TNF-alpha stimulates activation of pro-MMP2 in human skin through NF-kappa B mediated induction of MT1-MMP”.

Journal of Cell Science 2001; 114(Pt 1):131-139.

4. Yuan-Ping Han, Tai-Lan Tuan, Huayang Wu, Michael Hughes, Warren L. Garner. “TGF-beta and TNF-alpha mediated induction and proteolytic activation of MMP-9 in human skin”.

Journal of Biological Chemistry. 2001, vol.276 (25); 22341-22350.

5. Yuan-Ping Han, Micheal W. Hughes, Yih-Dar Nien and Warren L. Garner.

“IL-8-Stimulated Expression of Urokinase-Type Plasminogen Activator in Human Skin and Human Epidermal Cells”.

Journal of Surgery Research. 2002 Aug;106(2):328.

6. Mei Chen, Fritz K. Costa, Christopher R. Lindvay, Yuan-Ping Han, and David T. Woodley.

“The Recombinant Expression of Full-length Type VII Collagen and

Characterization of Molecular Mechanisms Underlying Dystrophic Epidermolysis

Bullosa”.

Journal of Biological Chemistry. 2002, vol. 277: 2118-2124.

7. Yuan-Ping Han, Yih-Dar Nien and Warren L.Garner.

“Recombinant human platelet-derived growth factor and transforming growth factor-beta mediated contraction of human dermal fibroblast populated lattices is inhibited by Rho/GTPase inhibitor but not require phosphatidylinositol-3u2019 kinase”.

Wound Repair and Regeneration. 2002, vol. 10, 169-176.

8. Yuan-Ping Han*, Yih-Dar Nien and Warren L.Garner.

“TNF-alpha mediated proteolytic activation of pro-MMP-9 in human skin is controlled by down regulation of the tissue inhibitor, TIMP-1 and mediated by tissue bound chymotrypsin-like proteinase”.

Journal of Biological Chemistry. 2002, 277: 27319-27327.

9. Yuan-Ping Han, Yih-Dar Nien and Warren L.Garner.

“Fibrinogen inhibits fibroblast-mediated contraction of collagen”.

Wound Repair and Regeneration. 2003 Sep;11(5):380-385.

10. Yuan-Ping Han*, Ling Zhou, Jiaohong Wang, Shigang Xiong, Warren L. Garner, Samuel W. French, Hidekazu Tsukamoto.

“Essential role of matrix metalloproteinases in interleukin-1 induced myofibrobalstic activation of hepatic stellate cell in collagen”.

Journal of Biological Chemistry. 2004, vol. 279, 4820-4828

11. Yuan-Ping Han, Downey S and Warren L.Garner.

“Interleukin-1alpha-induced proteolytic activation of metalloproteinase-9 by human skin”.

Surgery. 2005 Nov;138(5):932-9.

12. Yuan-Ping Han*.

“Matrix metalloproteinases, the pros and cons, in liver fibrosis”.

Journal of Gastroenterology & Hepatology. 2006 Oct; 21 Suppl 3:S88-91.

13. Yuan-Ping Han*, Chunli Yan, Ling Zhou, Lan Qin, and Hidekazu Tsukamoto.

“A Matrix Metalloproteinase-9 Activation Cascade by Hepatic Stellate Cells in Trans-differentiation in the hree-dimensional Extracellular Matrix”.

Journal of Biological Chemistry. 2007 Apr 27;282(17):12928-39

14. Goldberg MT, Han YP, Yan C, Shaw MC, Garner WL.

“TNF-alpha Suppresses alpha-Smooth Muscle Actin Expression in Human Dermal Fibroblasts: An Implication for Abnormal Wound Healing”.

Journal of Investigative Dermatology. 2007 May 31;127 (11):2645-55

15. Cheng JH, She H, Han YP, Wang J, Xiong S, Asahina K, Tsukamoto H.

“Wnt antagonism inhibits hepatic stellate cell activation and liver fibrosis”.

American Journal of Physiololy, (Gastrointest Liver Physiol) 2007, Nov 15; [Epub ahead of print] PMID: 18006602

16. Yuan-Ping Han*, Chunli Yan and Warren L Garner.

“Proteolytic Activation of Matrix Metalloproteinase-9 in Skin Wound Healing Is Inhibited by alpha-1-Antichymotrypsin”.

Journal of Investigative Dermatology. 2008 September; 128(9): 2334u20132342.

17. Chunli Yan, Ling Zhou, and Yuan-Ping Han*.

“Contribution of hepatic stellate cells and matrix metalloproteinase-9 in acute liver failure”.

Liver International. 2008 May 26. [Epub ahead of print].

18. Cheng CF, Fan J, Fedesco M, Guan S, Li Y, Bandyopadhyay B, Birght AM, Yerushalmi D, Liang M, Chen, Han YP, Woodley DT, Li W.

“Transforming growth factor alpha (TGFalpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGFbeta-rich environment during wound healing”.

Molecular Cell Biolology. 2008 May;28(10):3344-58. Epub 2008 Mar 10, MID:18332123.

19. Ling Zhou, Chunli Yan, Wei Li, Yujiro Kida, Warren L. Garner and Yuan-Ping Han*.

“p21 activated kinase (PAK) controls expression of MMP-9”.

BMC Immunology 2009, 10:15,19 March

20. Roben L. Gieling, Wallace, K. and Yuan-Ping Han*

“Participation of Interleukin-1 in Liver Injury induced Fibrosis”.

American Journal of Physiology, (Gastrointest Liver Physiol) . 2009, vol. 296,1324-31

21. MJ Reiss, Yuan-Ping Han, E Garcia, YK Hong, and WL Garner.

“ 1-Antichymotrypsin activity correlates with and may modulate matrix metalloproteinase-9 in human acute wounds ”.

Wound Healing and Regeneration, 2009, Published Online: May 20 2009, p 418-426

22. Shengwen Calvin Li, Yuan-Ping Han, Brent A. Dethlefs and William Gunter Loudon.

“Therapeutic Window of Stem Cell Potential for Targeting Pediatric Malignant Brain Tumor: An Opportunity for Stem Cell Therapy”.

Stem Cell Review and Reports, 2009, vol.5, issue 4, p446

23. MJ Reiss, Yuan-Ping Han, E Garcia, YK Hong, and WL Garner.

“Excessive Amount of Matrix Metalloproteinase-9 Delays Wound Healing in a Murine Wound Model”.

Surgery, 2010, February, Volume 147, Issue 2, Pages 295-302

24. Keigo Machida, Hidekazu Tsukamoto, Jian-Chang Liu, Yuan-Ping Han, Sugantha Govindarajan, Michael Lai, Shizuo Akira, James Ou, “c-Jun mediates HCV hepatocarcinogenesis through STAT3 and nitric oxide-dependent impairment of oxidative DNA repair”.

Hepatology, 2010 Aug;52(2):480-92

25. Chunli Yang, Wesley Grimm, Warren Garner, and Yuan-Ping Han*,

“Tumor necrosis factor-alpha induced epithelial-to-mesencymal transition in human skin fibrogenesis is mediated by bone morphogenetin protein-2”.

American Journal of Pathology, 2010, May. 176: 2247-2258. (Cover story)

26. Lan Qin and Yuan-Ping Han*.

“Epigenetic Repression of Matrix Metalloproteinases in Myofibroblastic Hepatic Stellate Cells through Histone Deacetylases 4,Implication in Tissue Fibrosis ”.

American Journal of Pathology, 2010, volume 177, Issue 4, page 1915 (Monthly Highlight)

27. Xiaohui Zhou, Zanxian Xia, Qin Lan, Julie Wang, Wenru Su,Yuan-Ping Han, Huimin Fan, Zhongmin Liu, William Stohl, and Song Guo Zheng.

“BAFF Promotes Th17 Cells and Aggravates Experimental Autoimmune Encephalomyelitis”.

PloS One, 2011; 6(8): Published online 2011 August. doi: 10.1371, PMCID: PMC3163640

28. Yujiro Kida, Zan Xian Xia, Sujun Zheng, Nick M. Mordwinkin, Stan G. Louie, Song Guo Zheng, Min Feng, Hongbo Shi, Zhongping Duan, and Yuan-Ping Han*. “Interleukin-1 as an injury signal mobilizes retinylesters in hepatic stellate cells through down regulation of lecithin retinol acyltransferase”.

PLoS One, 2011. 6(11): e26644. doi:10.1371/journal.pone.0026644

29. Ling Lu, Jilin Ma, Zhiyuan Li, Qin Lan, Maogen Chen, Ya Liu, Zanxian Xia, Julie Wang, Yuan-Ping Han, Wei Shi, Valerie Quesniaux, Bernhard Ryffel, David Brand, Bin Li, Zhongmin Liu, Song Guo Zheng.

“All-Trans Retinoic Acid Promotes TGF-β-Induced Tregs via Histone Modification but Not DNA Demethylation on Foxp3 Gene Locus”.

PloS One, 2011; 6(9): e24590. doi:10.1371/journal.pone.0024590.

30. Liyan Chen, Feng Ren, Haiyan Zhang, Tao Wen, Zhengfu Piao, Li Zhou, Sujun Zheng, Jing Zhang, Yu Chen, Yuanping Han, Zhongping Duan, Yingji Ma.

“Inhibition of Glycogen Synthase Kinase 3b Ameliorates D-GalN/LPS-Induced Liver Injury by Reducing Endoplasmic Reticulum Stress-Triggered Apoptosis”

PLoS One, 2011. September 2012 | Volume 7 | Issue 9 | e45202

31. Yuan-Ping Han*, Ming Kong, Sujun Zheng, Yang Ren, Hongbo Shi, and Zhongping Duan.

“Vitamin D In Liver Diseases: From Mechanisms to Clinical Trials”.

Journal of Gastroenterology and Hepatology. 2013; 28, Suppl.1: 49u201355

32. Ling Lu, Min Feng, Lan Qin et al., Yuan-Ping Han*.

“Restoration of intrahepatic regulatory T cells through MMP-9/13-dependent activation of TGF-β is critical for immune homeostasis following acute liver injury”.

Journal of Molecular Cell Biology. (2013) 5 (6): 369-379

33. Wei L, Ren F, Zhang X, Wen T, Shi H, Zheng S, Zhang J, Chen Y, Han Y, Duan Z.

“Oxidative stress promotes D-GalN/LPS-induced acute hepatotoxicity by increasing glycogen synthase kinase 3β activity”.

Inflammation Research. 2014 Jun; 63(6):485-94. doi: 10.1007/s00011-014-0720-x. Epub 2014 Feb 16.

34. Kong M, Zhu L, Bai L, Zhang X, Chen Y, Liu S, Zheng S, Pandol SJ, Han YP, Duan Z.

“Vitamin D deficiency promotes nonalcoholic steatohepatitis through impaired enterohepatic circulation in animal model”.

American Journal of Physiology, Gastrointest Liver Physiol. 2014 Nov 1;307(9):G883-93. doi: 10.1152/ajpgi.00427.2013. Epub 2014 Sep 11.

PMID: 25214402 [PubMed - in process]

35. Liu L, Ye TH, Han YP, Song H, Zhang YK, Xia Y, Wang NY, Xiong Y, Song XJ, Zhu YX, Li de L, Zeng J, Ran K, Peng CT, Wei YQ, Yu LT.

“Reductions in myeloid derived suppressor cells and lung metastases using AZD4547 Treatment of a metastatic murine breast tumor model”.

Cell Physiol Biochem. 2014;33(3):633-45. doi: 10.1159/000358640. Epub 2014 Mar 4. PMID: 24642893 [PubMed - in process]

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