About

Wei Ying is an Assistant Professor in the Department of Medicine at UC San Diego, located at 9500 Gilman Drive, La Jolla, CA 92093. Her research focuses on the mechanisms underlying maternal obesity-induced microbial DNA accumulation in fetuses and offspring, as well as how hepatocyte extracellular microRNAs mediate peripheral insulin sensitivity. She has been recognized with several awards, including the UCSD NIDDK K99/R00 award from 2018 to 2023 and the American Heart Association Postdoctoral Fellowship from 2016 to 2018. Her work involves investigating the roles of extracellular vesicles, microRNAs, and immune cell functions in metabolic regulation and obesity-related diseases.

Research topics

• Internal medicine
• Biology
• Medicine
• Endocrinology
• Biochemistry
• Immunology
• Cell biology
• Genetics
• Computational biology
• Cancer research

Selected publications

• Regulation of iron metabolism and its implications in cancer and metabolic disease

  KOBRA Reports · 2026-04-22

  articleOpen access
  PublisherDOI

• Context-dependent regulation of iron metabolism in macrophages

  KOBRA Reports · 2026-04-23

  articleOpen access

  Iron is an essential element that supports a wide range of biological processes.Cellular iron is mainly imported in the ferric (Fe 3+ ) form via transferrin receptor protein 1 (TFR1) and reduced to ferrous (Fe 2+ ) ion which is utilized as the labile iron pool or stored in ferritin.Through multiple regulatory mechanisms, cells control labile iron levels to sustain fundamental processes such as DNA synthesis and mitochondrial respiration and to prevent iron-induced oxidative stress.Given the fundamental role of iron in cellular physiology, recent studies have increasingly focused on how iron regulates immune cell function and development.In particular, macrophages have been extensively studied due to their pivotal role in iron handling, storage, and recycling.Although numerous studies suggest that elevated intracellular iron promotes macrophage polarization toward pro-inflammatory phenotypes, emerging evidence indicates that the consequences of iron regulation in macrophages are more complex and highly disease-dependent.In this review, we summarize current knowledge on the interplay between iron metabolism and macrophage biology and highlight recent findings that reveal context-specific mechanisms across diverse physiology and pathological environment.

  PublisherOA PDFDOI

• ATF4 drives regulatory T cell functional specification in homeostasis and obesity

  Science Immunology · 2025-03-14 · 9 citations

  articleOpen accessSenior authorCorresponding

  Regulatory T cells (T regs ) have diverse functional specification in homeostasis and disease. However, how liver T regs function and are transcriptionally regulated in obesity is not well understood. Here, we identified that effector T regs expressing activating transcription factor 4 (ATF4) were enriched in the livers of obese mice. ATF4 was critical for driving an effector T reg transcriptional program, and ATF4-expressing T regs promoted the development of obesity-induced liver fibrosis by enhancing transforming growth factor–β activation via integrin αvβ8. T reg -specific deletion of Atf4 resulted in reduced liver T regs and attenuation of obesity-induced liver abnormalities. Furthermore, ATF4 was required to promote the differentiation of nonlymphoid tissue T reg precursors under steady state. These findings demonstrate that ATF4 is important for regulating T reg functional specification in homeostasis and obesity.

  PublisherOA PDFDOI

• Adipose Tissue Macrophages in Metabolic Dysfunction–Associated Steatohepatitis Secrete Extracellular Vesicles That Activate Liver Fibrosis in Obese Male Mice

  Gastroenterology · 2025-04-09 · 16 citations

  article
  PublisherDOI

• Overview of the hazardous impacts of metabolism-disrupting chemicals on the progression of fatty liver diseases

  Molecular & Cellular Toxicology · 2025-02-27 · 12 citations

  articleOpen accessCorresponding

  Background: Given the global increase in obesity, metabolic dysfunction-associated steatotic liver disease (MASLD) is a major health concern. Because the liver is the primary organ for xenobiotic metabolism, the impact of environmental stressors on liver homeostasis and MASLD has garnered significant interest over the past few decades. The concept of metabolism-disrupting chemicals (MDCs) has been introduced to underscore the importance of environmental factors in metabolic homeostasis. Recent epidemiological and biological studies suggest a causal link between exposure to MDCs and prevalence and progression of MASLD. Objective: This review aims to introduce the emerging concept of MDCs and their representative toxic mechanisms. In particular, this review focuses on broadening the understanding of their impacts on MASLD or metabolic dysfunction-associated steatohepatitis (MASH) progression. Result: Recent research has highlighted the environmental contaminants, such as heavy metals, microplastics, and pesticides, have the potential to influence hepatic metabolism and aggravate MASLD/MASH progression. These MDCs not only directly affect lipid metabolism in hepatocytes but also affect other cell types, such as immune cells and stellate cells, as well as the gut-liver axis. Conclusion: Collectively, these findings contribute to establishing a well-defined adverse outcome pathway and identify novel therapeutic options for liver diseases associated with pollutants.

  PublisherOA PDFDOI

• Adipose tissue macrophage-derived miR-690 modulates adipocyte precursor cell maintenance and adipogenesis

  Molecular Metabolism · 2025-09-03 · 1 citations

  articleOpen accessSenior author

  Obesity is intricately linked to various metabolic diseases; however, some individuals maintain metabolic health despite being classified as obese. A critical factor underlying this paradox is the expansion of white adipose tissue (WAT), which can occur through two mechanisms: hypertrophy (the enlargement of existing fat cells) and hyperplasia (the formation of new fat cells from adipocyte precursor cells, or APCs). Hyperplasia is regarded as a healthier mode of WAT expansion, as it tends to reduce inflammation and protect against insulin resistance. Thus, interventions that promote hyperplasia over hypertrophy could improve metabolic health in obese individuals. In this study, we investigate the role of microRNA-690 (miR-690), an anti-inflammatory and insulin-sensitizing molecule, in maintaining the APC population and facilitating the healthy expansion of epididymal WAT (eWAT). Our findings indicate that in lean mice, macrophages support the APC population by transferring miR-690 to APCs. However, during obesity, the recruitment of pro-inflammatory lipid-associated macrophages (LAMs) to eWAT diminishes miR-690 delivery to APCs, impairing adipogenesis and leading to unhealthy WAT expansion. We demonstrate that strategies aimed at increasing the availability of miR-690 to APCs or mimicking its effects can restore APC functionality. Additionally, mutations in Nadk, the target of miR-690, were shown to mitigate the adverse effects of obesity on APC maintenance in eWAT. These findings suggest that targeting the miR-690-Nadk axis in APCs may provide novel therapeutic strategies to promote healthy adipose tissue expansion and protect against obesity-related metabolic diseases.

  PublisherDOI

• Obesity rewires CD8+ T cell iron metabolism in adipose tissue to fuel metabolic inflammation

  Metabolism · 2025-11-17 · 1 citations

  articleSenior author
  PublisherDOI

• Neutrophils preserve energy storage in sympathetically activated adipocytes

  Nature · 2025-12-10 · 2 citations

  articleOpen access
  PublisherOA PDFDOI

• Restoring SRSF3 in Kupffer cells attenuates obesity-related insulin resistance

  Hepatology · 2024-03-08 · 6 citations

  articleOpen accessSenior author

  BACKGROUND AND AIMS: In obesity, depletion of KCs expressing CRIg (complement receptor of the Ig superfamily) leads to microbial DNA accumulation, which subsequently triggers tissue inflammation and insulin resistance. However, the mechanism underlying obesity-mediated changes in KC complement immune functions is largely unknown. APPROACH AND RESULTS: Using KC-specific deactivated Cas9 transgenic mice treated with guide RNA, we assessed the effects of restoring CRIg or the serine/arginine-rich splicing factor 3 (SRSF3) abundance on KC functions and metabolic phenotypes in obese mice. The impacts of weight loss on KC responses were evaluated in a diet switch mouse model. The role of SRSF3 in regulating KC functions was also evaluated using KC-specific SRSF3 knockout mice. Here, we report that overexpression of CRIg in KCs of obese mice protects against bacterial DNA accumulation in metabolic tissues. Mechanistically, SRSF3 regulates CRIg expression, which is essential for maintaining the CRIg+ KC population. During obesity, SRSF3 expression decreases, but it is restored with weight loss through a diet switch, normalizing CRIg+ KCs. KC SRSF3 is also repressed in obese human livers. Lack of SRSF3 in KCs in lean and obese mice decreases their CRIg+ population, impairing metabolic parameters. During the diet switch, the benefits of weight loss are compromised due to SRSF3 deficiency. Conversely, SRSF3 overexpression in obese mice preserves CRIg+ KCs and improves metabolic responses. CONCLUSIONS: Restoring SRSF3 abundance in KCs offers a strategy against obesity-associated tissue inflammation and insulin resistance by preventing bacterial DNA accumulation.

  PublisherOA PDFDOI

• Exosome-Mediated Impact on Systemic Metabolism

  Annual Review of Physiology · 2024-02-12 · 82 citations

  articleOpen access

  Exosomes are small extracellular vesicles that carry lipids, proteins, and microRNAs (miRNAs). They are released by all cell types and can be found not only in circulation but in many biological fluids. Exosomes are essential for interorgan communication because they can transfer their contents from donor to recipient cells, modulating cellular functions. The miRNA content of exosomes is responsible for most of their biological effects, and changes in exosomal miRNA levels can contribute to the progression or regression of metabolic diseases. As exosomal miRNAs are selectively sorted and packaged into exosomes, they can be useful as biomarkers for diagnosing diseases. The field of exosomes and metabolism is expanding rapidly, and researchers are consistently making new discoveries in this area. As a result, exosomes have great potential for a next-generation drug delivery platform for metabolic diseases.

  PublisherOA PDFDOI

Recent grants

• Adipose tissue macrophages secrete exosome-miRs as paracrine/endocrine molecules to directly modulate insulin target cell function in response to obesity

  NIH · $739k · 2020–2024

• The mechanisms underlying maternal obesity-induced microbial DNA accumulation in fetus and offspring metabolic abnormalities

  NIH · $435k · 2022–2025

• Mechanisms by which hepatocyte extracellular miRNAs mediate peripheral insulin sensitivity

  NIH · $2.0M · 2021–2027

• Adipose tissue macrophages secrete exosome-miRs as paracrine/endocrine molecules to directly modulate insulin target cell function in response to obesity

  NIH · $180k · 2018–2020

Frequent coauthors

• Beiyan Zhou

  University of Connecticut

  27 shared

• Yudong Ji

  Xinxiang Medical University

  23 shared

• Rongxiu Zheng

  Tianjin Medical University General Hospital

  23 shared

• Zhenlong Luo

  Tongji Hospital

  19 shared

• Stephen Safe

  Texas A&M University

  19 shared

• Patali S. Cheruku

  18 shared

• Geert van den Bogaart

  University of Groningen

  18 shared

• Sushil K. Mahata

  University of California, San Diego

  18 shared

Education

• Postdoc fellow, Medicine

  University of California San Diego

  2017

• Ph.D.

  Texas A&M University

  2015

• M.S.

  Kansas State University

  2011

• M.S.

  China Agricultural University

  2009

• B.S.

  China Agricultural University

  2007

Awards & honors

• NIDDK K99/R00 award (2018 - 2023)
• American Heart Association Postdoctoral Fellowship (2016 - 2…
• American Heart Association Predoctoral Fellowship (2013 - 20…