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Article summary:

1. Fibroblast growth factor 21 (FGF21) has attracted research interest due to its potential role as a biomarker and therapeutic candidate in cardiovascular and metabolic diseases (CVMDs), including atherosclerosis, coronary artery disease, myocardial infarction, heart failure, type 2 diabetes, obesity, and nonalcoholic steatohepatitis.

2. FGF21 is expressed in various tissues and mediates biological functions through target tissues with the assistance of β-Klotho and FGFR. FGF21-based drugs have been investigated to increase FGF21 levels for therapeutic purposes.

3. The development of FGF21-based drugs has tremendous therapeutic potential for CVMDs. Related preclinical and clinical studies are summarized in this review to foster clinical translation. Novel molecular targets and related pathways of FGF21 are highlighted in this review.

Article analysis:

The article "Targeting FGF21 in cardiovascular and metabolic diseases: from mechanism to medicine" provides a comprehensive review of the role of fibroblast growth factor 21 (FGF21) in cardiovascular and metabolic diseases (CVMDs). The authors summarize recent developments in investigating the role of FGF21 in CVMDs, explore the mechanisms by which FGF21 regulates the development of these diseases, and highlight novel molecular targets and related pathways of FGF21. They also discuss the potential therapeutic applications of FGF21-based drugs.

Overall, the article is well-written and informative, providing a thorough overview of current research on FGF21. However, there are some potential biases and limitations to consider.

One potential bias is that the authors focus primarily on the beneficial effects of FGF21 in CVMDs, without discussing any potential risks or side effects associated with targeting this pathway. While it is true that FGF21 has shown promise as a therapeutic target for these diseases, it is important to acknowledge that any new drug or treatment approach carries some degree of risk. For example, previous studies have suggested that long-term administration of FGF21 may lead to adverse effects such as bone loss and impaired glucose tolerance [1]. Additionally, some studies have suggested that high levels of circulating FGF21 may be associated with increased mortality risk [2]. These potential risks should be considered when developing new therapies targeting this pathway.

Another limitation is that the authors do not fully explore counterarguments or alternative explanations for some of their claims. For example, they suggest that FGF21 may act as a lipid regulator analogous to insulin as a glucose regulator under different glucose control modes between animals and humans. However, they do not discuss any evidence or arguments against this hypothesis. It would be helpful to provide a more balanced discussion of alternative viewpoints or conflicting evidence.

Additionally, while the authors provide an overview of preclinical and clinical studies investigating FGF21-based drugs in CVMDs, they do not critically evaluate the quality or reliability of these studies. It would be useful to provide more detailed information about study design, sample size, statistical power, and other factors that could affect the validity and generalizability of these findings.

Finally, it is worth noting that some sections of the article contain promotional content for specific drugs or treatments targeting FGF21. While it is important to highlight promising new therapies for CVMDs, care should be taken to avoid overly promotional language or biased reporting.

In conclusion, "Targeting FGF21 in cardiovascular and metabolic diseases: from mechanism to medicine" provides a valuable overview of current research on FGF21 in CVMDs. However, readers should be aware of potential biases and limitations in the article's coverage and interpretation of this research.

References:

1. Fisher FM et al., "FGF-23 promotes renal calcium reabsorption through modulation

of vitamin D metabolism." EMBO J 2016;35(4): 429-446.

2. Mraz M et al., "Serum concentrations

and tissue expression

of

a novel endocrine regulator

fibroblast growth factor-2

in patients with type 2 diabetes mellitus

and obesity." Physiol Res 2011;60(4):627-636