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Mechanism and therapeutic strategies of depression after myocardial infarction

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Abstract

Depression resulted as an important factor associated with the myocardial infarction (MI) prognosis. Patients with MI also have a higher risk for developing depression. Although the issue of depression after MI has become a matter of clinical concern, the molecular mechanism underlying depression after MI remains unclear, whereby several strategies suggested have not got ideal effects, such as selective serotonin reuptake inhibitors. In this review, we summarized and discussed the occurrence mechanism of depression after MI, such as 5-hydroxytryptamine (5-HT) dysfunction, altered hypothalamus-pituitary-adrenal (HPA) axis function, gut microbiota imbalance, exosomal signal transduction, and inflammation. In addition, we offered a succinct overview of treatment, as well as some promising molecules especially from natural products for the treatment of depression after MI.

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Abbreviations

AADC:

Amino acid decarboxylase

ACTH:

Adrenocortical hormones

AMI:

Acute myocardial infarction

BBB:

Blood–brain barrier

BDNF:

Brain-derived neurotrophic factor

CAD:

Coronary artery disease

CVD:

Cardiovascular disease

COR:

Cortisol

CRH:

Corticotropin-releasing hormone

CREATE:

Cardiovascular Risk Reduction by Early Anemia Treatment with Epoetin Beta

DHA:

Docosahexaenoic acid

ESC:

Embryonic stem cells

ENRICHD:

Enhancing Recovery in Coronary Heart Disease

EPA:

Eicosapentaenoic acid

GF:

Germfree

GRK2:

G protein–coupled receptor kinase 2

GRs:

Glucocorticoid receptors

GHSR:

Growth hormone secretagogue receptor

GFS:

Ginseng fruit saponins

HADS:

Hospital Anxiety and Depression Scale

HDRS:

Depression Rating Scale

HPA:

Hypothalamus–pituitary–adrenal

IDO:

Indoleamine 2,3-dioxygenase

IL-6:

Interleukin-6

IL-1β:

Interleukin-1β

IL-17a:

Interleukin-17a

L-Trp:

L-Tryptophan

MADRS:

Montgomery–Asberg Depression Rating Scale

MI:

Myocardial infarction

MAO:

Monoamine oxidase A

MSCs:

Mesenchymal stem cells

PHQ:

Patient Health Questionnaire

PI3K:

Phosphoinositide 3-kinase

PTX:

Pentoxifylline

PSD95:

Postsynaptic density protein-95

PrP:

Prion protein

SADHART:

Sertraline Antidepressant Heart Attack Randomized Trial

SERT:

Serotonin transporter

SSRIs:

Selective serotonin reuptake inhibitors

SYP:

Synaptophysin

SDF1:

Stromal-derived factor 1

TNF-α:

Necrosis factor alpha

TrkB:

Tyrosine kinase receptors

TPH:

Tryptophan hydroxylase

TMAO:

Trimethylamine N-oxide

TMA:

Trimethylamine

VEGF:

Vascular endothelial growth factor

5-HIAA:

5-Hydroxyindoleacetic acid

5-HT:

5-Hydroxytryptamine

5-HTP:

5-Hydroxytryptophan

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Funding

This work was supported by the National Natural Science Foundation of China (No. 81803765), the Natural Science Foundation of Guangdong Province (No. 1914050000567), the Special Innovation Projects of Universities in Guangdong Province (No. 2019KTSCX027), Scientific Research Team Training Project of GZUCM (No. 2019KYTD201), and Guangdong Key Laboratory for Translational Cancer Research of Chinese Medicine (No. 2018B030322011).

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YY took charge of the literature review and drafted the manuscript. XPL, SXC, MZX, and ZQL helped to draft the manuscript. JYL and YYC conceived, designed, and finalized the draft. All authors read and approved the final manuscript.

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Correspondence to Jingyan Li or Yuanyuan Cheng.

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Yang, Y., Li, X., Chen, S. et al. Mechanism and therapeutic strategies of depression after myocardial infarction. Psychopharmacology 238, 1401–1415 (2021). https://doi.org/10.1007/s00213-021-05784-0

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