Fibroblast growth factor 21 in patients with cardiac cachexia: a possible role of chronic inflammation

Holm, Magnus; Christensen, H. E.; Rasmussen, Jeppe Nørgaard; Johansen, Marie Louise; Schou, Morten; Faber, Jens; Kistorp, Caroline

doi:10.1002/ehf2.12502

Cited by 24 publications

(23 citation statements)

References 41 publications

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“…FGF21 can be induced by inflammatory stimuli. 507 – 509 FGF21 is associated with the suppression of cardiac, renal, and hepatic inflammation. 510 – 512 FGF21 is thought to be one of the potential immunotherapy targets for cardiovascular inflammation and pancreatic fibrogenesis as it can alter the macrophage polarization states.…”

Section: Fgf Signaling In Inflammatory Responsementioning

confidence: 99%

FGF/FGFR signaling in health and disease

Xie

Yang

et al. 2020

Sig Transduct Target Ther

511

391

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Growing evidences suggest that the fibroblast growth factor/FGF receptor (FGF/FGFR) signaling has crucial roles in a multitude of processes during embryonic development and adult homeostasis by regulating cellular lineage commitment, differentiation, proliferation, and apoptosis of various types of cells. In this review, we provide a comprehensive overview of the current understanding of FGF signaling and its roles in organ development, injury repair, and the pathophysiology of spectrum of diseases, which is a consequence of FGF signaling dysregulation, including cancers and chronic kidney disease (CKD). In this context, the agonists and antagonists for FGF-FGFRs might have therapeutic benefits in multiple systems.

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Section: Fgf Signaling In Inflammatory Responsementioning

confidence: 99%

FGF/FGFR signaling in health and disease

Xie

Yang

et al. 2020

Sig Transduct Target Ther

511

391

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“…Among patients with HFrEF and HFpEF, serum levels of FGF-21 were positively associated with echocardiographic parameters of diastolic function, LV end-diastolic pressure, and NT-pro-BNP levels [ 88 – 90 ], as well as with IL-6 levels and lower skeletal muscle mass [ 91 ]. Conflicting results in the presence of the strong correlation between serum levels of FGF-21 and NT-pro-BNP are explained by adjustment of the data for cardiac cachexia [ 91 , 92 ]. There was strong correlation between circulating levels of FGF-21 and NT-pro-BNP in HFrEF patients without cardiac cachexia, but no correlation between these biomarkers was noticed in those who had HFrEF with cardiac cachexia [ 93 ].…”

Section: Myokines In Hf Myopathymentioning

confidence: 99%

Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes

Berezin

Lichtenauer

2021

Disease Markers

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Heart failure (HF) is a global medical problem that characterizes poor prognosis and high economic burden for the health system and family of the HF patients. Although modern treatment approaches have significantly decreased a risk of the occurrence of HF among patients having predominant coronary artery disease, hypertension, and myocarditis, the mortality of known HF continues to be unacceptably high. One of the most important symptoms of HF that negatively influences tolerance to physical exercise, well-being, social adaptation, and quality of life is deep fatigue due to HF-related myopathy. Myopathy in HF is associated with weakness of the skeletal muscles, loss of myofibers, and the development of fibrosis due to microvascular inflammation, metabolic disorders, and mitochondrial dysfunction. The pivotal role in the regulation of myocardial and skeletal muscle rejuvenation, attenuation of muscle metabolic homeostasis, and protection against ischemia injury and apoptosis belongs to myokines. Myokines are defined as a wide spectrum of active molecules that are directly synthesized and released by both cardiac and skeletal muscle myocytes and regulate energy homeostasis in autocrine/paracrine manner. In addition, myokines have a large spectrum of pleiotropic capabilities that are involved in the pathogenesis of HF including cardiac remodeling, muscle atrophy, and cardiac cachexia. The aim of the narrative review is to summarize the knowledge with respect to the role of myokines in adverse cardiac remodeling, myopathy, and clinical outcomes among HF patients. Some myokines, such as myostatin, irisin, brain-derived neurotrophic factor, interleukin-15, fibroblast growth factor-21, and growth differential factor-11, being engaged in the regulation of the pathogenesis of HF-related myopathy, can be detected in peripheral blood, and the evaluation of their circulating levels can provide new insights to the course of HF and stratify patients at higher risk of poor outcomes prior to sarcopenic stage.

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“…In up to 20% of heart failure patients with reduced EF, which is accompanied by an inflammatory losing weight syndrome, namely cardiac cachexia, the serum level of FGF21 is also increased ( Refsgaard Holm et al, 2019 ). Augmented circulating FGF21 levels are also evident in other patients with non-acute and acute MI ( Zhang W. et al, 2015 ).…”

Section: Roles Of Fgf In Cardiac Pathophysiology and Repairmentioning

confidence: 99%

The Multifunctional Contribution of FGF Signaling to Cardiac Development, Homeostasis, Disease and Repair

Khosravi

Ahmadvand

Bellusci

et al. 2021

Front. Cell Dev. Biol.

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The current focus on cardiovascular research reflects society’s concerns regarding the alarming incidence of cardiac-related diseases and mortality in the industrialized world and, notably, an urgent need to combat them by more efficient therapies. To pursue these therapeutic approaches, a comprehensive understanding of the mechanism of action for multifunctional fibroblast growth factor (FGF) signaling in the biology of the heart is a matter of high importance. The roles of FGFs in heart development range from outflow tract formation to the proliferation of cardiomyocytes and the formation of heart chambers. In the context of cardiac regeneration, FGFs 1, 2, 9, 16, 19, and 21 mediate adaptive responses including restoration of cardiac contracting rate after myocardial infarction and reduction of myocardial infarct size. However, cardiac complications in human diseases are correlated with pathogenic effects of FGF ligands and/or FGF signaling impairment. FGFs 2 and 23 are involved in maladaptive responses such as cardiac hypertrophic, fibrotic responses and heart failure. Among FGFs with known causative (FGFs 2, 21, and 23) or protective (FGFs 2, 15/19, 16, and 21) roles in cardiac diseases, FGFs 15/19, 21, and 23 display diagnostic potential. The effective role of FGFs on the induction of progenitor stem cells to cardiac cells during development has been employed to boost the limited capacity of postnatal cardiac repair. To renew or replenish damaged cardiomyocytes, FGFs 1, 2, 10, and 16 were tested in (induced-) pluripotent stem cell-based approaches and for stimulation of cell cycle re-entry in adult cardiomyocytes. This review will shed light on the wide range of beneficiary and detrimental actions mediated by FGF ligands and their receptors in the heart, which may open new therapeutic avenues for ameliorating cardiac complications.

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Fibroblast growth factor 21 in patients with cardiac cachexia: a possible role of chronic inflammation

Cited by 24 publications

References 41 publications

FGF/FGFR signaling in health and disease

FGF/FGFR signaling in health and disease

Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes

The Multifunctional Contribution of FGF Signaling to Cardiac Development, Homeostasis, Disease and Repair

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