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Lei Yang

Researcher at University of Pittsburgh

Publications -  49
Citations -  6099

Lei Yang is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Cellular differentiation & Induced pluripotent stem cell. The author has an hindex of 28, co-authored 49 publications receiving 5503 citations. Previous affiliations of Lei Yang include Icahn School of Medicine at Mount Sinai & Chinese Academy of Sciences.

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Human cardiovascular progenitor cells develop from a KDR + embryonic-stem-cell-derived population

TL;DR: Analysis of the development of the cardiovascular lineages in human embryonic stem cell differentiation cultures identifies a human cardiovascular progenitor that defines one of the earliest stages of human cardiac development.
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A myocardial lineage derives from Tbx18 epicardial cells

TL;DR: The identification in mouse of a previously unknown cardiac myocyte lineage that derives from the proepicardial organ is reported, which provides a theoretical framework for applying these progenitors to effect cardiac repair and regeneration.
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Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome

TL;DR: In vitro-derived cardiomyocytes from LEOPARD syndrome iPSCs are larger, have a higher degree of sarcomeric organization and preferential localization of NFATC4 in the nucleus when compared with cardiomeocytes derived from human embryonic stem cells or wild-type iPSC derived from a healthy brother of one of the LEopARD syndrome patients, which correlate with a potential hypertrophic state.
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Repopulation of decellularized mouse heart with human induced pluripotent stem cell-derived cardiovascular progenitor cells.

TL;DR: It is shown that the seeded multipotential cardiovascular progenitor cells migrate, proliferate and differentiate in situ into cardiomyocytes, smooth muscle cells and endothelial cells to reconstruct the decellularized hearts.
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Induction of acetylcholinesterase expression during apoptosis in various cell types

TL;DR: The studies demonstrate that AChE is potentially a marker and a regulator of apoptosis and that blocking the expression of A ChE with antisense inhibited apoptosis.