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The role of P53 up-regulated modulator of apoptosis (PUMA) in ovarian development, cardiovascular and neurodegenerative diseases

Journal

APOPTOSIS
Volume 26, Issue 5-6, Pages 235-247

Publisher

SPRINGER
DOI: 10.1007/s10495-021-01667-z

Keywords

PUMA; Apoptosis; Excessive cell death; Ovary; Cardiovascular disease; Neurodegenerative disease

Funding

  1. Ministry of Agriculture and Rural Affairs of the People's Republic of China [C0201600746]
  2. Jiangsu Overseas Research and Training Program for University Prominent Young and Middle-Aged Teachers and Presidents [[2015]1507]
  3. National Natural Science Foundation of China [NSFC: 31301945]
  4. Fundamental Research Funds for Central Universities [KJQN201403]

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PUMA, a pro-apoptotic member of the BCL-2 family, is a direct transcriptional target of P53 and plays a critical role in various cell apoptotic processes, including ovarian development and cardiovascular neurodegenerative diseases. Recent studies have shown that PUMA-mediated apoptotic pathways contribute to understanding the regulation of cell death mechanisms.
P53 up-regulated modulator of apoptosis (PUMA), a pro-apoptotic BCL-2 homology 3 (BH3)-only member of the BCL-2 family, is a direct transcriptional target of P53 that elicits mitochondrial apoptosis under treatment with radiation and chemotherapy. It also induces excessive apoptosis in cardiovascular and/or neurodegenerative diseases. PUMA has been found to play a critical role in ovarian apoptosis. In the present paper, we review the progress of the study in PUMA over the past two decades in terms of its inducement and/or amplification of programmed cell death and describe recent updates to the understanding of both P53-dependent and P53-independent PUMA-mediated apoptotic pathways that are implicated in physiology and pathology, including the development of the ovary and cardiovascular and neurodegenerative diseases. We propose that PUMA may be a key regulator during ovary development, provide a model for PUMA-mediated apoptotic pathways, including intrinsic and extrinsic apoptotic pathways.

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