α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor

Anni Suominen; Guillem Saldo Rubio; Saku Ruohonen; Zoltán Szabó; Lotta Pohjolainen; Bishwa Ghimire; Suvi T. Ruohonen; Karla Saukkonen; Jani Ijas; Sini Skarp; Leena Kaikkonen; Minying Cai; Sharon L. Wardlaw; Heikki Ruskoaho; Virpi Talman; Eriika Savontaus; Risto Kerkelä; Petteri Rinne

doi:10.1038/s44319-024-00109-6

α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor

Anni Suominen
, Guillem Saldo Rubio
, Saku Ruohonen
, Zoltán Szabó
, Lotta Pohjolainen
, Bishwa Ghimire
, Suvi T. Ruohonen
, Karla Saukkonen
, Jani Ijas
, Sini Skarp
, Leena Kaikkonen
, Minying Cai
, Sharon L. Wardlaw
, Heikki Ruskoaho
, Virpi Talman
, Eriika Savontaus
, Risto Kerkelä
, Petteri Rinne

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

(Figure presented.) α-Melanocyte-stimulating hormone (α-MSH) regulates several physiological functions by interacting with melanocortin receptors (MC1-R–MC5-R). This study shows that α-MSH is expressed in the heart and it protects against pathological cardiac remodeling by activating MC5-R in cardiomyocytes. α-MSH production declines in the failing mouse heart. Pharmacological administration of α-MSH alleviates pathological cardiac hypertrophy induced by pressure overload. The protective effects of α-MSH are mediated by the melanocortin 5 receptor (MC5-R), which is expressed in mouse and human cardiac myocytes. Silencing MC5-R in cardiomyocytes renders mice susceptible to cardiac hypertrophy and fibrosis after pressure overload.

Original language	English (US)
Pages (from-to)	1987-2014
Number of pages	28
Journal	EMBO Reports
Volume	25
Issue number	4
DOIs	https://doi.org/10.1038/s44319-024-00109-6
State	Published - Apr 12 2024

Keywords

Fibrosis
Heart Failure
Hypertrophy
Melanocortin Receptor
Melanocyte-stimulating Hormone

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Genetics

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10.1038/s44319-024-00109-6

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Suominen, A., Saldo Rubio, G., Ruohonen, S., Szabó, Z., Pohjolainen, L., Ghimire, B., Ruohonen, S. T., Saukkonen, K., Ijas, J., Skarp, S., Kaikkonen, L., Cai, M., Wardlaw, S. L., Ruskoaho, H., Talman, V., Savontaus, E., Kerkelä, R., & Rinne, P. (2024). α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor. EMBO Reports, 25(4), 1987-2014. https://doi.org/10.1038/s44319-024-00109-6

Suominen, A, Saldo Rubio, G, Ruohonen, S, Szabó, Z, Pohjolainen, L, Ghimire, B, Ruohonen, ST, Saukkonen, K, Ijas, J, Skarp, S, Kaikkonen, L, Cai, M, Wardlaw, SL, Ruskoaho, H, Talman, V, Savontaus, E, Kerkelä, R & Rinne, P 2024, 'α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor', EMBO Reports, vol. 25, no. 4, pp. 1987-2014. https://doi.org/10.1038/s44319-024-00109-6

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abstract = "(Figure presented.) α-Melanocyte-stimulating hormone (α-MSH) regulates several physiological functions by interacting with melanocortin receptors (MC1-R–MC5-R). This study shows that α-MSH is expressed in the heart and it protects against pathological cardiac remodeling by activating MC5-R in cardiomyocytes. α-MSH production declines in the failing mouse heart. Pharmacological administration of α-MSH alleviates pathological cardiac hypertrophy induced by pressure overload. The protective effects of α-MSH are mediated by the melanocortin 5 receptor (MC5-R), which is expressed in mouse and human cardiac myocytes. Silencing MC5-R in cardiomyocytes renders mice susceptible to cardiac hypertrophy and fibrosis after pressure overload.",

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AU - Szabó, Zoltán

AU - Pohjolainen, Lotta

AU - Ghimire, Bishwa

AU - Ruohonen, Suvi T.

AU - Saukkonen, Karla

AU - Ijas, Jani

AU - Skarp, Sini

AU - Kaikkonen, Leena

AU - Cai, Minying

AU - Wardlaw, Sharon L.

AU - Ruskoaho, Heikki

AU - Talman, Virpi

AU - Savontaus, Eriika

AU - Kerkelä, Risto

AU - Rinne, Petteri

PY - 2024/4/12

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N2 - (Figure presented.) α-Melanocyte-stimulating hormone (α-MSH) regulates several physiological functions by interacting with melanocortin receptors (MC1-R–MC5-R). This study shows that α-MSH is expressed in the heart and it protects against pathological cardiac remodeling by activating MC5-R in cardiomyocytes. α-MSH production declines in the failing mouse heart. Pharmacological administration of α-MSH alleviates pathological cardiac hypertrophy induced by pressure overload. The protective effects of α-MSH are mediated by the melanocortin 5 receptor (MC5-R), which is expressed in mouse and human cardiac myocytes. Silencing MC5-R in cardiomyocytes renders mice susceptible to cardiac hypertrophy and fibrosis after pressure overload.

AB - (Figure presented.) α-Melanocyte-stimulating hormone (α-MSH) regulates several physiological functions by interacting with melanocortin receptors (MC1-R–MC5-R). This study shows that α-MSH is expressed in the heart and it protects against pathological cardiac remodeling by activating MC5-R in cardiomyocytes. α-MSH production declines in the failing mouse heart. Pharmacological administration of α-MSH alleviates pathological cardiac hypertrophy induced by pressure overload. The protective effects of α-MSH are mediated by the melanocortin 5 receptor (MC5-R), which is expressed in mouse and human cardiac myocytes. Silencing MC5-R in cardiomyocytes renders mice susceptible to cardiac hypertrophy and fibrosis after pressure overload.

KW - Fibrosis

KW - Heart Failure

KW - Hypertrophy

KW - Melanocortin Receptor

KW - Melanocyte-stimulating Hormone

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UR - https://www.scopus.com/pages/publications/85186865841#tab=citedBy

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DO - 10.1038/s44319-024-00109-6

M3 - Article

C2 - 38454158

SN - 1469-221X

VL - 25

SP - 1987

EP - 2014

JO - EMBO Reports

JF - EMBO Reports

IS - 4

ER -

α-Melanocyte-stimulating hormone alleviates pathological cardiac remodeling via melanocortin 5 receptor

Abstract

Keywords

ASJC Scopus subject areas

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