Milad Rezvani

ORCID: 0000-0002-9550-8725
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About
Contact & Profiles
Research Areas
  • Liver physiology and pathology
  • Pancreatic function and diabetes
  • Liver Disease Diagnosis and Treatment
  • Organ Transplantation Techniques and Outcomes
  • Pluripotent Stem Cells Research
  • Hepatitis C virus research
  • Metabolism and Genetic Disorders
  • HIV, Drug Use, Sexual Risk
  • Neonatal Respiratory Health Research
  • Bipolar Disorder and Treatment
  • COVID-19 and Mental Health
  • Drug-Induced Hepatotoxicity and Protection
  • COVID-19 and healthcare impacts
  • Stress Responses and Cortisol
  • Neuroscience of respiration and sleep
  • Liver Diseases and Immunity
  • Neonatal Health and Biochemistry
  • Electroconvulsive Therapy Studies
  • Renal and related cancers
  • Cellular Mechanics and Interactions
  • MicroRNA in disease regulation
  • Congenital Diaphragmatic Hernia Studies
  • Genetic and Kidney Cyst Diseases
  • Tryptophan and brain disorders
  • Childhood Cancer Survivors' Quality of Life

Berlin Institute of Health at Charité - Universitätsmedizin Berlin
2023-2024

Humboldt-Universität zu Berlin
2023-2024

Charité - Universitätsmedizin Berlin
2022-2024

Freie Universität Berlin
2023-2024

Cincinnati Children's Hospital Medical Center
2021-2024

Semnan University of Medical Sciences
2024

Harvard University
2021

Boston Medical Center
2021

Boston University
2021

Boston Children's Hospital
2021

Matrix rigidity has important effects on cell behavior and is increased during liver fibrosis; however, its effect primary hepatocyte function unknown. We hypothesized that matrix in fibrotic livers would activate mechanotransduction hepatocytes lead to inhibition of liver-specific functions. To determine the physiologically relevant ranges stiffness at cellular level, we performed detailed atomic force microscopy analysis across lobules from normal livers. determined was around 150 Pa 1-6...

10.1002/hep.28450 article EN Hepatology 2016-01-12

Background Injured or reactive biliary epithelial cells participate in most chronic liver injuries a process referred to as ductular reaction, which involves multicellular interactions with marked local infiltration of macrophages and fibrogenic cell activation. The direct roles shaping their cellular niche remain unknown. Objective We aimed at investigating the effects cell-derived acute phase response protein orosomucoid 2 (ORM2) monocyte/macrophage injury. Design Transcriptome data sets...

10.1136/gutjnl-2024-334425 article EN Gut 2025-04-08

Background . Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of premature birth, characterized by impaired alveolar development and inflammation. Pathomechanisms contributing to BPD are poorly understood. However, it assumed that genetic factors predispose other pulmonary diseases preterm neonates, such as neonatal respiratory distress syndrome (RDS). For association studies, genes upregulated during alveolarization major candidates for analysis, example, matrix...

10.1155/2013/932356 article EN cc-by Disease Markers 2013-01-01

SUMMARY The fetal liver is a hematopoietic organ, hosting diverse and evolving progenitor population. While human organoids derived from pluripotent stem cells (PSCs) mimic aspects of embryonic development, they typically lack the complex niche interaction between hepatic development. We describe generation Fetal Liver-like Organoids (FLOs), that model hepato-hematopoietic interactions previously characterized in mouse models. Developing FLOs first integrate yolk sac-like hemogenic...

10.1101/2024.10.11.617794 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-12

Metabolic dysfunction-associated steatotic liver disease (MASLD)—generally the consequence of Western lifestyle and genetic predispositions—is most common cause fibrosis. The spectrum progression ranges from steatosis to mixed inflammatory cell infiltration (steatohepatitis) and, eventually, cirrhosis. This process also rewires transcriptional network within hepatocytes—the main parenchymal type. Thereby, usually silent developmental pathways reemerge in hepatocytes, including YAP-TAZ...

10.1016/j.omtm.2023.101182 article EN cc-by Molecular Therapy — Methods & Clinical Development 2024-01-01

Abstract Metabolic dysfunction-associated steatotic liver disease (MASLD) is a complex, multifactorial condition influenced by genetic predisposition, inter-organ signaling, and immune cell infiltration. The difficulty of modeling the complex nature makes it increasingly challenging to identify treatments that intercept its progression. Here, we show suitability cumulative injury toward steatohepatitis from hepatocyte-like cells (HLCs) generated human induced pluripotent stem (iPSCs). These...

10.1101/2024.10.10.617610 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-11

10.1016/j.jpeds.2021.03.061 article EN The Journal of Pediatrics 2021-06-22

10.1016/j.jpeds.2021.07.050 article EN The Journal of Pediatrics 2021-09-22
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