Molecular Mechanisms Underlying Pluripotency and Self-Renewal of Embryonic Stem Cells

Fahimeh Varzideh; Jessica Gambardella; Urna Kansakar; Stanislovas S Jankauskas; Gaetano Santulli

doi:10.3390/ijms24098386

Molecular Mechanisms Underlying Pluripotency and Self-Renewal of Embryonic Stem Cells

Int J Mol Sci. 2023 May 7;24(9):8386. doi: 10.3390/ijms24098386.

Authors

Fahimeh Varzideh¹, Jessica Gambardella², Urna Kansakar¹, Stanislovas S Jankauskas¹, Gaetano Santulli^{1

2}

Affiliations

¹ Department of Medicine (Division of Cardiology), Wilf Family Cardiovascular Research Institute, Einstein Institute for Aging Research, Institute for Neuroimmunology and Inflammation (INI), Albert Einstein College of Medicine, New York, NY 10461, USA.
² Department of Molecular Pharmacology, Einstein-Mount Sinai Diabetes Research Center (ES-DRC), Fleischer Institute for Diabetes and Metabolism (FIDAM), Albert Einstein College of Medicine, New York, NY 10461, USA.

Abstract

Embryonic stem cells (ESCs) are derived from the inner cell mass (ICM) of the blastocyst. ESCs have two distinctive properties: ability to proliferate indefinitely, a feature referred as "self-renewal", and to differentiate into different cell types, a peculiar characteristic known as "pluripotency". Self-renewal and pluripotency of ESCs are finely orchestrated by precise external and internal networks including epigenetic modifications, transcription factors, signaling pathways, and histone modifications. In this systematic review, we examine the main molecular mechanisms that sustain self-renewal and pluripotency in both murine and human ESCs. Moreover, we discuss the latest literature on human naïve pluripotency.

Keywords: CRISPR/Cas9; Klf4; Oct4; embryonic stem cell (ESC); epigenetics; histone modifications; human ESC (hESC) vs. mouse ESC (mESC); naïve vs. primed pluripotency; pluripotent stem cells (PSC); self-renewal.

Publication types

Systematic Review
Review

MeSH terms

Animals
Blastocyst
Cell Differentiation
Embryonic Stem Cells*
Human Embryonic Stem Cells* / metabolism
Humans
Mice
Signal Transduction
Transcription Factors / metabolism

Substances

Transcription Factors

Grants and funding

The Santulli’s Lab is currently supported in part by the National Institutes of Health (NIH): National Center for Advancing Translational Sciences (NCATS: UL1-TR002556-06, UM1-TR004400), National Heart, Lung, and Blood Institute (NHLBI: R01-HL164772, R01-HL159062, R01-HL146691, T32-HL144456), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK: R01-DK123259, R01-DK033823), to G.S., by the Diabetes Action Research and Education Foundation (to G.S.), and by the Monique Weill-Caulier and Irma T. Hirschl Trusts (to G.S.). F.V. is supported in part by a postdoctoral fellowship of the American Heart Association (AHA-22POST915561). J.G. is supported by a postdoctoral fellowship of the American Heart Association (AHA-20POST35211151). S.S.J. is supported in part by a postdoctoral fellowship of the American Heart Association (AHA-21POST836407). U.K. is supported in part by a postdoctoral fellowship of the American Heart Association (AHA-23POST1026190).