About

Hang Lu is a scholar specializing in science, health, environmental, and risk communication (ComSHER) with a focus on media psychology. His research program aims to understand how different audience segments respond to media messages related to SHER issues and how these messages can be crafted to maximize their effectiveness. He has developed four main research streams that address psychological mechanisms influencing the effectiveness of media messages on individual behaviors and policy support: the role of emotions in audience responses, predictors of information seeking, processing, and sharing behaviors, media effects on (de)stigmatization, and the prosocial use of artificial intelligence in sensitive and controversial domains. Lu's research has been conducted across various contexts, including emerging infectious diseases such as COVID-19 and Zika virus, climate change, vaccination, genetically modified food, obesity, addiction, mental well-being, emerging technologies, and human-wildlife conflicts. He has published extensively in peer-reviewed journals across disciplines and has received numerous top paper awards from professional associations. Currently, Lu serves as the chair of the Environmental Communication Division of the International Communication Association and directs the Media and Risk (MaR) lab at the University of Michigan. Prior to his current position, he was a postdoctoral fellow at the Annenberg Public Policy Center of the University of Pennsylvania.

Research topics

• Biology
• Computer Science
• Internal medicine
• Genetics
• Computational biology
• Medicine
• Cell biology
• Pharmacology
• Cardiology
• Chemistry
• Biochemistry
• Bioinformatics

Selected publications

• Metabolic reprogramming in aortic diseases: insights from metabolomics and therapeutic opportunities

  Medical Review · 2026-03-19

  articleOpen accessSenior author

  Aortic diseases (aortic aneurysm, aortic dissection, atherosclerosis) represent a substantial clinical and economic burden due to the lack of effective early diagnostic tools and mechanism-based therapies. Metabolomics, the systematic study of low-molecular-weight metabolites, has emerged as a powerful approach for elucidating pathogenesis, screening candidate biomarkers, and discovering novel drug targets. Rather than merely cataloging metabolic perturbations, this review highlights how metabolic reprogramming, particularly involving amino acid pathways, mitochondrial dysfunction, and gut microbiota-derived metabolites, actively drives aortic pathology. While specific metabolites (e.g., succinate and trimethylamine N-oxide) show promises as prognostic biomarkers, their greatest value lies in revealing actionable therapeutic nodes. Although challenges remain regarding metabolite identification, biological heterogeneity, and clinical translation, continued technological advances and integrative multi-omics approaches offer clear pathways to overcome these barriers. Ultimately, we posit that prioritizing these convergent metabolic axes, especially the gut-vascular interface, could unlock next-generation precision therapies that transcend the limitations of conventional hemodynamic management.

  PublisherDOI

• Role of Caveolae and Caveolin in Vascular Physiology and Pathology

  Journal of the American Heart Association · 2026-02-12 · 1 citations

  articleOpen accessSenior authorCorresponding

  Caveolae, 50-100 nm cholesterol-rich plasma membrane invaginations, serve as critical signaling hubs in vascular cells. These structures-scaffolded by caveolin proteins (CAV1, CAV2, CAV3) and regulated by Cavins-orchestrate membrane dynamics, mechanotransduction, and lipid trafficking in endothelial cells, smooth muscle cells, and macrophages. In vascular physiology, caveolae modulate vascular tone, regulate lipoprotein metabolism, and mediate mechanosensation. In pathology, caveolae are implicated in atherosclerosis, pulmonary hypertension, and diabetic vasculopathy. This review synthesizes advances in caveolae biology, highlighting their roles in vascular homeostasis and disease. We propose caveolae-targeted therapies as promising strategies for cardiovascular disorders, contingent on resolving context-dependent signaling complexity.

  PublisherDOI

• TCF7L2 promotes abdominal aortic aneurysm through smooth muscle cell-mediated extracellular matrix remodeling

  JCI Insight · 2026-04-30

  articleOpen access

  Abdominal aortic aneurysm (AAA) lacks effective pharmacological therapies. Here, we investigate transcription factor 7-like 2 (TCF7L2), a genetic locus associated with both thoracic and abdominal aortic aneurysms, to elucidate its role in AAA pathogenesis. Integrating summary-data-based Mendelian randomization (SMR) with single-cell RNA sequencing (scRNA-seq) of human and mouse aortas, we identify TCF7L2 as a gene enriched in vascular smooth muscle cells (VSMCs) and causally linked to AAA development. Smooth muscle cell-specific TCF7L2 knockout significantly attenuates AAA formation across three distinct murine models (Ang II infusion-, BAPN/Ang II co-administration-, and elastase-induced AAA), independent of systemic blood pressure or lipid levels. Mechanistic studies reveal that TCF7L2 directly upregulates MMP14 and downregulates TIMP3 expression in vitro and in vivo, driving MMP2-mediated extracellular matrix (ECM) degradation. Concurrently, TCF7L2 represses integrin β1 (ITGB1) expression, reducing VSMC adhesion to the ECM. Collectively, these findings identify TCF7L2 as a key driver of pathological vascular remodeling in AAA, suggesting that targeting TCF7L2 may offer a novel therapeutic strategy for limiting AAA progression.

  PublisherDOI

• SWAP70 Promotes Atherosclerosis Via Endothelial CAV1 Nuclear Translocation

  Circulation Research · 2026-01-14

  article

  BACKGROUND: Atherosclerosis, the leading cause of coronary artery disease, is initiated and exacerbated by disturbed blood flow and chronic endothelial inflammation. SWAP70 (switch-associated protein 70), a multifunctional signaling adaptor, has been genetically linked to coronary artery disease susceptibility via the risk allele rs10840293. However, its precise role in atherogenesis remains poorly understood. METHODS: We employed both endothelial cell-specific Swap70 overexpression and knockout mouse models, alongside lentiviral overexpression and siRNA-mediated SWAP70 knockdown in human umbilical vein endothelial cells, to investigate the functional role of SWAP70 in vascular inflammation and plaque development. In vitro assays subjected human umbilical vein endothelial cells to oscillatory shear stress or proinflammatory cytokines, followed by evaluation of adhesion molecule and chemokine expression. Mechanistic studies were performed using coimmunoprecipitation, proximity ligation assay, mimetic peptide interference, RNA sequencing, and ChIP-qPCR analyses. RESULTS: SWAP70 expression was significantly upregulated in human atherosclerotic plaques and in human umbilical vein endothelial cells exposed to oscillatory shear stress compared with laminar shear stress. On oscillatory shear stress stimulation, SWAP70 bound to the scaffolding domain of CAV1 (caveolin-1) to facilitate its nuclear translocation, thereby enhancing transcription of key inflammatory mediators, including adhesion molecules and chemokines. In vitro, SWAP70 knockdown suppressed oscillatory shear stress and TNFα (tumor necrosis factor-α)-induced proinflammatory gene expression. In vivo, endothelial-specific deletion of Swap70 attenuated high-fat diet-induced atherosclerotic lesion formation, reduced vascular inflammation, and improved plaque stability. Conversely, overexpression of Swap70 amplified inflammatory responses and worsened atherogenic outcomes. CONCLUSIONS: Our findings identify SWAP70 as a mechano-responsive regulator of endothelial inflammation and atherosclerosis, acting through a novel mechanism involving CAV1 nuclear translocation. Targeting the SWAP70-CAV1 signaling axis represents a promising therapeutic strategy for mitigating vascular inflammation and attenuating the progression of atherosclerotic cardiovascular disease.

  PublisherDOI

• Novel gene regulatory networks identified in response to nitro-conjugated linoleic acid in human endothelial cells

  Zenodo (CERN European Organization for Nuclear Research) · 2025-09-30

  datasetOpen accessSenior author

  A distinct transcriptome regulated by NO_2-CLA was revealed in primary human coronary artery endothelial cells (HCAECs) through RNA sequencing.

  PublisherDOI

• Case Report: A FBN1 frameshift-and-nonsense mutation and aortic dissection in Marfan syndrome

  Frontiers in Cardiovascular Medicine · 2025-04-23 · 1 citations

  articleOpen accessCorresponding

  Background Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder primarily affecting the cardiovascular, ocular, and skeletal systems. Cardiovascular complications are the leading cause of mortality in MFS. Mutations in the FBN1 gene, which encodes fibrillin-1, a critical extracellular matrix protein, are the predominant cause of the disorder. Case presentation On March 11, 2024, we diagnosed a 30-year-old female proband with MFS based on the revised Ghent criteria, presenting with aortic root aneurysm, aortic dissection, multiple skeletal abnormalities, and a family history of MFS. Whole-exome sequencing followed by Sanger sequencing confirmation identified a novel inherited insertion mutation (c.4991dupA) in exon 40 of the FBN1 gene. We performed valve-sparing aortic root replacement (David Procedure) and total aortic arch replacement using a tetrafurcated graft, along with the implantation of a specially designed frozen elephant trunk in the descending aorta (Sun's Procedure). Postoperatively, the patient underwent biweekly clinical follow-ups for three months. No treatment-related adverse events were reported during the monitoring period. Conclusion The diagnosis of MFS requires an integrated approach, combining clinical manifestations, imaging studies, and genetic analysis. This novel mutation is associated with severe skeletal manifestations and life-threatening cardiovascular abnormalities, underscoring its clinical relevance. Its association with aggressive phenotypes enhances genotype-phenotype correlations. Importantly, these findings highlight the imperative need for early intervention in high-risk individuals by bridging genetic discovery to clinical practice.

  PublisherOA PDFDOI

• Angiogenesis in Atrial Fibrillation: A Literature Review

  Biomedicines · 2025-06-06

  reviewOpen accessSenior authorCorresponding

  Atrial fibrillation (AF), the most prevalent clinically significant cardiac arrhythmia, is characterized by chaotic atrial electrical activity and currently affects an estimated 2.5-3.5% of the global population. Its pathogenesis involves ion channel dysfunction, inflammatory cascades, and structural remodeling processes, notably fibrosis. Angiogenesis, the physiological/pathological process of new blood vessel formation, plays a multifaceted role in AF progression. This review synthesizes evidence highlighting angiogenesis's dual role in AF pathogenesis: while excessive or dysregulated angiogenesis promotes atrial remodeling through fibrosis, and electrical dysfunction via VEGF, ANGPT, and FGF signaling pathways, compensatory angiogenesis exerts protective effects by improving tissue perfusion to alleviate ischemia and inflammation. Therapeutically, targeting angiogenic pathways-particularly VEGF-represents a promising strategy for modulating structural remodeling; however, non-selective VEGF inhibition raises safety concerns due to cardiovascular toxicity, necessitating cautious exploration. Emerging evidence highlights that anti-cancer agents (e.g., ibrutinib, bevacizumab) impair endothelial homeostasis and elevate AF risk, underscoring the need for cardio-oncology frameworks to optimize risk-benefit ratios. Preclinical studies on angiogenesis inhibitors and gene therapies provide mechanistic insights, but clinical validation remains limited. Future research should prioritize elucidating mechanistic complexities, developing biomarker refinement, and implementing interdisciplinary strategies integrating single-cell sequencing with cardio-oncology principles. This review emphasizes the imperative to clarify angiogenic mechanisms, optimize therapeutic strategies, and balance pro-arrhythmic versus compensatory angiogenesis, in pursuit of personalized AF management.

  PublisherOA PDFDOI

• Novel gene regulatory networks identified in response to nitro-conjugated linoleic acid in human endothelial cells

  Zenodo (CERN European Organization for Nuclear Research) · 2025-09-30

  datasetOpen accessSenior author

  A distinct transcriptome regulated by NO_2-CLA was revealed in primary human coronary artery endothelial cells (HCAECs) through RNA sequencing.

  PublisherDOI

• CRISPR‐MI and scRNA‐Seq Reveal TREM2's Function in Monocyte Infiltration and Macrophage Apoptosis During Abdominal Aortic Aneurysm Development

  Advanced Science · 2025-10-07 · 2 citations

  articleOpen access1st authorCorresponding

  Abdominal aortic aneurysm (AAA) is a life-threatening aortic disease without effective medication. The infiltration of monocytes into the aortic wall is critical for AAA development, but the genes and pathways regulating this process remain to be elucidated. A novel method is developed for in vivo genome-wide CRISPR/Cas9 screening of monocyte infiltration (CRISPR-MI). By combining CRISPR-MI with single-cell RNA sequencing (scRNA-Seq), this study finds that Triggering receptor expressed on myeloid cells 2 (Trem2) is a negative regulator of monocyte infiltration into the aortic wall in early AAA induction. Trem2 knockout (KO) increases the expression of adhesion molecules, chemotactic receptors, and cytokines in monocytes. Trem2 KO promotes monocyte adhesion and migration in vitro and increases monocyte infiltration into the aortic wall in vivo. However, Trem2 KO attenuates AAA development because of prominent macrophage death at the late stage. In conclusion, CRISPR-MI is a powerful tool for studying genes underlying monocyte infiltration in disease conditions in vivo. These findings reveal a dichotomous role of Trem2 in monocyte recruitment and macrophage survival during AAA.

  PublisherDOI

• Hypertriglyceridemia as a Key Contributor to Abdominal Aortic Aneurysm Development and Rupture: Insights From Genetic and Experimental Models

  Circulation · 2025-08-05 · 10 citations

  articleOpen access

  BACKGROUND: Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease with no effective pharmacological treatments. The causal role of triglycerides (TGs) in AAA development remains unclear and controversial. METHODS: Mendelian randomization was applied to assess causal relationships between lipoproteins, circulating proteins, metabolites, and the risk of AAA. To test the hypothesis that elevated plasma TG levels accelerate AAA development, we used Lpl -deficient, Apoa5 -deficient, and human APOC3 transgenic mice, which display varying degrees of hypertriglyceridemia. Mechanistic studies were performed using RNA sequencing and Western blot analysis of palmitate-treated vascular smooth muscle cells and validated in vivo by local overexpression of key mediator in the suprarenal abdominal aorta. Antisense oligonucleotides targeting Angptl3 were administered to reduce TG levels and assess therapeutic potential in human APOC3 transgenic and Apoe -deficient mice. RESULTS: Mendelian randomization analyses integrating genetic, proteomic, and metabolomic data identified causal relationships between elevated TG-rich lipoproteins, TG metabolism–related proteins/metabolites, and AAA risk. In the angiotensin II infusion AAA model, most Lpl -deficient mice with severely elevated TG concentrations died of aortic rupture. Similarly, Apoa5 -deficient mice with moderately elevated TG levels developed accelerated AAA, and human APOC3 transgenic mice with dramatically elevated TG levels exhibited aortic dissection and rupture. Mechanistically, elevated TG and palmitate inhibited lysyl oxidase (LOX) maturation and reduced LOX activity. Locally overexpressing lysyl oxidase eliminated the proaneurysmal effect of hypertriglyceridemia in human APOC3 transgenic mice. Moreover, an Angptl3 -targeting antisense oligonucleotide profoundly attenuated AAA progression in both human APOC3 transgenic and Apoe -deficient mice. CONCLUSIONS: These findings identify hypertriglyceridemia as a key contributor to AAA pathogenesis and suggest that targeting TG-rich lipoproteins may be a promising therapeutic strategy for AAA.

  PublisherOA PDFDOI

Frequent coauthors

• Jifeng Zhang

  University of Michigan–Ann Arbor

  68 shared

• Y. Eugene Chen

  Michigan Center for Translational Pathology

  60 shared

• Yanbo Fan

  40 shared

• Wenying Liang

  University of Michigan–Ann Arbor

  39 shared

• Guizhen Zhao

  University of Houston

  36 shared

• Minerva T. Garcia-Barrio

  University of Michigan–Ann Arbor

  35 shared

• Huilun Wang

  University of Virginia

  32 shared

• Yanhong Guo

  University of Michigan–Ann Arbor

  31 shared

Education

• PhD, Physiology

  University of Michigan

  2019

• B.S, National School of Development

  Peking Univeristy

  2014

• B.S, Clinical Medicine

  Peking University Health Science Centre

  2014

Awards & honors

• a dozen top paper awards from the International Communicatio…
• a dozen top paper awards from the Association for Education…
• a dozen top paper awards from the Society for Risk Analysis…