The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy
Abstract Cardiac hypertrophy can lead to heart failure and cardiovascular events and has become a research hotspot in the field of cardiovascular disease. Despite extensive and in‐depth research, the pathogenesis of cardiac hypertrophy is far from being fully understood. Increasing evidence has show...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-12-01
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| Series: | ESC Heart Failure |
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| Online Access: | https://doi.org/10.1002/ehf2.13065 |
| _version_ | 1818977080060149760 |
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| author | Wei Yu Chunjuan Chen Jidong Cheng |
| author_facet | Wei Yu Chunjuan Chen Jidong Cheng |
| author_sort | Wei Yu |
| collection | DOAJ |
| description | Abstract Cardiac hypertrophy can lead to heart failure and cardiovascular events and has become a research hotspot in the field of cardiovascular disease. Despite extensive and in‐depth research, the pathogenesis of cardiac hypertrophy is far from being fully understood. Increasing evidence has shown that the transcription factor forkhead box protein O 1 (FoxO1) is closely related to the occurrence and development of cardiac hypertrophy. This review summarizes the current literature on the role and molecular mechanism of FoxO1 in cardiac hypertrophy. We searched the database MEDLINE via PubMed for available evidence on the effect of FoxO1 on cardiac hypertrophy. FoxO1 has many effects on multiple diseases, including cardiovascular diseases, diabetes, cancer, aging, and stem cell activity. Recent studies have shown that FoxO1 plays a critical role in the development of cardiac hypertrophy. Evidence for this relationship includes the following. (i) FoxO1 can regulate cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy and (ii) is controlled by several upstream signalling molecules (e.g. phosphatidylinositol 3‐kinase/Akt, AMP‐activated protein kinase, and sirtuins) and regulates many downstream transcription proteins (e.g. ubiquitin ligases muscle RING finger 1/muscle atrophy F‐box, calcineurin/nuclear factor of activated T cells, and microRNAs). In response to stress or external stimulation (e.g. low energy, oxidative stress, or growth factor signalling), FoxO1 undergoes post‐translational modification and transfers from the cytoplasm to nucleus, thus regulating the expression of a series of target genes in myocardium that are involved in cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy. (iii) Finally, targeted regulation of FoxO1 is an effective method of intervening in myocardial hypertrophy. The information reviewed here should be significant for understanding the roles of FoxO1 in cardiac hypertrophy and should contribute to the design of further studies related to FoxO1 and the hypertrophic response. It should also shed light on a potential treatment for cardiac hypertrophy. |
| first_indexed | 2024-12-20T16:22:03Z |
| format | Article |
| id | doaj.art-ff83c556402549728f0ff624830db219 |
| institution | Directory Open Access Journal |
| issn | 2055-5822 |
| language | English |
| last_indexed | 2024-12-20T16:22:03Z |
| publishDate | 2020-12-01 |
| publisher | Wiley |
| record_format | Article |
| series | ESC Heart Failure |
| spelling | doaj.art-ff83c556402549728f0ff624830db2192022-12-21T19:33:35ZengWileyESC Heart Failure2055-58222020-12-01763497350410.1002/ehf2.13065The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophyWei Yu0Chunjuan Chen1Jidong Cheng2Department of Internal Medicine Xiang'an Hospital of Xiamen University Xiamen 361102 ChinaDepartment of Cardiology Second Affiliated Hospital of Shantou University Medical College 69 Dong Xia North Road Shantou 515041 ChinaDepartment of Internal Medicine Xiang'an Hospital of Xiamen University Xiamen 361102 ChinaAbstract Cardiac hypertrophy can lead to heart failure and cardiovascular events and has become a research hotspot in the field of cardiovascular disease. Despite extensive and in‐depth research, the pathogenesis of cardiac hypertrophy is far from being fully understood. Increasing evidence has shown that the transcription factor forkhead box protein O 1 (FoxO1) is closely related to the occurrence and development of cardiac hypertrophy. This review summarizes the current literature on the role and molecular mechanism of FoxO1 in cardiac hypertrophy. We searched the database MEDLINE via PubMed for available evidence on the effect of FoxO1 on cardiac hypertrophy. FoxO1 has many effects on multiple diseases, including cardiovascular diseases, diabetes, cancer, aging, and stem cell activity. Recent studies have shown that FoxO1 plays a critical role in the development of cardiac hypertrophy. Evidence for this relationship includes the following. (i) FoxO1 can regulate cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy and (ii) is controlled by several upstream signalling molecules (e.g. phosphatidylinositol 3‐kinase/Akt, AMP‐activated protein kinase, and sirtuins) and regulates many downstream transcription proteins (e.g. ubiquitin ligases muscle RING finger 1/muscle atrophy F‐box, calcineurin/nuclear factor of activated T cells, and microRNAs). In response to stress or external stimulation (e.g. low energy, oxidative stress, or growth factor signalling), FoxO1 undergoes post‐translational modification and transfers from the cytoplasm to nucleus, thus regulating the expression of a series of target genes in myocardium that are involved in cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy. (iii) Finally, targeted regulation of FoxO1 is an effective method of intervening in myocardial hypertrophy. The information reviewed here should be significant for understanding the roles of FoxO1 in cardiac hypertrophy and should contribute to the design of further studies related to FoxO1 and the hypertrophic response. It should also shed light on a potential treatment for cardiac hypertrophy.https://doi.org/10.1002/ehf2.13065Cardiac hypertrophyHeart failurePathogenesisFoxO1Therapeutics |
| spellingShingle | Wei Yu Chunjuan Chen Jidong Cheng The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy ESC Heart Failure Cardiac hypertrophy Heart failure Pathogenesis FoxO1 Therapeutics |
| title | The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy |
| title_full | The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy |
| title_fullStr | The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy |
| title_full_unstemmed | The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy |
| title_short | The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy |
| title_sort | role and molecular mechanism of foxo1 in mediating cardiac hypertrophy |
| topic | Cardiac hypertrophy Heart failure Pathogenesis FoxO1 Therapeutics |
| url | https://doi.org/10.1002/ehf2.13065 |
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