The emerging role of leptin in obesity-associated cardiac fibrosis: evidence and mechanism

Mao, Yu; Zhao, Kun; Sheng, Yanhui

doi:10.1007/s11010-022-04562-6

Cited by 4 publications

(2 citation statements)

References 186 publications

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“…Indeed, we know that leptin is an adipose tissue-derived hormone [ 25 ] that has a pro-fibrotic action at the hepatic, renal, and myocardial levels; regulates skeletal muscle metabolism; and acts as a pro-angiogenic factor [ 25 ]. Leptin-induced fibrotic response is a complex process that involves multiple cells and is regulated by multiple molecular pathway (reviewed in Mao) [ 26 ]. Thus, the interaction of leptin with P3NP indicates that a fibrotic process is activated [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Muscle quality, physical performance, and comorbidity are predicted by circulating procollagen type III N-terminal peptide (P3NP): the InCHIANTI follow-up study

et al. 2023

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Sarcopenia is characterized by skeletal muscle quantitative and qualitative alterations. A marker of collagen turnover, procollagen type III N-terminal peptide (P3NP), seems to be related to those conditions. This study aims to assess the predictive role of P3NP in muscle density and physical performance changes. In the InCHIANTI study, a representative sample from the registry lists of two towns in Tuscany, Italy, was recruited. Baseline data was collected in 1998, and follow-up visits were conducted every 3 years. Out of the 1453 participants enrolled at baseline, this study includes 1052 participants. According to P3NP median levels, population was clustered in two groups; 544 (51.7%) of the 1052 subjects included were classified in the low median levels (LM-P3NP); at the baseline, they were younger, had higher muscle density, and performed better at the Short Physical Performance Battery (SPPB), compared to the high-median group (HM-P3NP).LM-P3NP cases showed a lower risk to develop liver chronic diseases, CHF, myocardial infarction, and osteoarthritis. HM-P3NP levels were associated with a longitudinal reduction of muscle density, and this effect was potentiated by the interaction between P3NP and leptin. Moreover, variation in physical performance was inversely associated with high level of P3NP, and directly associated with high fat mass, and with the interaction between P3NP and muscle density. Our data indicate that P3NP is associated with the aging process, affecting body composition, physical performance, and clinical manifestations of chronic degenerative age-related diseases.

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Section: Discussionmentioning

confidence: 99%

Muscle quality, physical performance, and comorbidity are predicted by circulating procollagen type III N-terminal peptide (P3NP): the InCHIANTI follow-up study

et al. 2023

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“…Induction of myocardial overexpression during ischemia and reperfusion has been shown to enhance myocardial remodelling, resulting in increased myocardial dysfunction [50]. Moreover, leptin has been shown to contribute to myocardial remodelling by stimulating myocardial fibrosis, thus further contributing to the development of heart failure [50,51].…”

Section: Leptin and Cardiac Hypertrophymentioning

confidence: 99%

Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin

Karmazyn,

Gan

2024

IJMS

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Since its initial discovery in 1994, the adipokine leptin has received extensive interest as an important satiety factor and regulator of energy expenditure. Although produced primarily by white adipocytes, leptin can be synthesized by numerous tissues including those comprising the cardiovascular system. Cardiovascular function can thus be affected by locally produced leptin via an autocrine or paracrine manner but also by circulating leptin. Leptin exerts its effects by binding to and activating specific receptors, termed ObRs or LepRs, belonging to the Class I cytokine family of receptors of which six isoforms have been identified. Although all ObRs have identical intracellular domains, they differ substantially in length in terms of their extracellular domains, which determine their ability to activate cell signalling pathways. The most important of these receptors in terms of biological effects of leptin is the so-called long form (ObRb), which possesses the complete intracellular domain linked to full cell signalling processes. The heart has been shown to express ObRb as well as to produce leptin. Leptin exerts numerous cardiac effects including the development of hypertrophy likely through a number of cell signaling processes as well as mitochondrial dynamics, thus demonstrating substantial complex underlying mechanisms. Here, we discuss mechanisms that potentially mediate leptin-induced cardiac pathological hypertrophy, which may contribute to the development of heart failure.

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The link between obesity and aging - insights into cardiac energy metabolism

Owesny,

Grune

2023

Mechanisms of Ageing and Development

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The emerging role of leptin in obesity-associated cardiac fibrosis: evidence and mechanism

Cited by 4 publications

References 186 publications

Muscle quality, physical performance, and comorbidity are predicted by circulating procollagen type III N-terminal peptide (P3NP): the InCHIANTI follow-up study

Muscle quality, physical performance, and comorbidity are predicted by circulating procollagen type III N-terminal peptide (P3NP): the InCHIANTI follow-up study

Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin

The link between obesity and aging - insights into cardiac energy metabolism

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