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Homovanillic acid improves anxiety by regulating F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury
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  • Published: 18 March 2026

Homovanillic acid improves anxiety by regulating F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury

  • Zhenfei Wu1 na1,
  • Zujuan Huang1 na1,
  • Fengpei Ding1 na1,
  • Hongbo Ma2,
  • Chuntao Deng4,
  • Changchun Zeng1,
  • Rong Chang1,
  • Wenbin Kuang3 &
  • …
  • Yanli Zhao1 na1 

Scientific Reports , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Cardiology
  • Diseases
  • Medical research
  • Neuroscience
  • Physiology

Abstract

The heart-brain axis is a significant contributor to morbidity and mortality following ischemic injury. Pathological and psychological changes in the heart can lead to anxiety, cognitive impairment, and brain injury. Cardiac injury releases a substantial number of metabolites into the peripheral circulation, which exacerbates brain damage and dysfunction. Homovanillic acid (HVA), a metabolite of dopamine (DA), plays a crucial role in behavioral symptoms. However, there are limited studies examining the effects of cardiac metabolites released from an injured heart on behavioral symptoms in human juveniles, particularly in those who have suffered from severe cardiovascular diseases since childhood in human models. To study the potential role of injured cardiac metabolites on human juveniles’ behaviors, we use neonatal mouse heart cryoinjury to verify the mechanisms of heart-brain interactions in our study. Here, downregulated cardiac heart HVA is enriched in neonatal mouse injured heart at day 7 after injury, and meanwhile HVA treatment changes the physiology of the body such as heart weight/body weight, brain weight/body weight and thymus weight/body weight in mouse juveniles with chronic mouse cardiac injury. Additionally, HVA administration mediates anxiety-like behavior in the same group. Microglia/macrophages contribute to brain development and functions, potentially influencing on human behaviors, which is associates with MCP-1 expression. Mechanistically, we identifies the number of F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury increases in HVA treatment, while there is no difference in mRNA and protein expression levels of MCP-1 at day 42 after injury. Thus, HVA may be a potential target in clinical behavioral symptoms with cardiovascular diseases.

Data availability

All data included in this study are available upon request by contact with the corresponding author.

References

  1. Xu, W. et al. Novel Pan-ERR agonists ameliorate heart failure through enhancing cardiac fatty acid metabolism and mitochondrial function. Circulation 149, 227–250. https://doi.org/10.1161/CIRCULATIONAHA.123.066542 (2024).

    Google Scholar 

  2. Walker, M. A. et al. Raising NAD(+) level stimulates short-chain dehydrogenase/reductase proteins to alleviate heart failure independent of mitochondrial protein deacetylation. Circulation 148, 2038–2057. https://doi.org/10.1161/CIRCULATIONAHA.123.066039 (2023).

    Google Scholar 

  3. Ritterhoff, J. & Tian, R. Metabolic mechanisms in physiological and pathological cardiac hypertrophy: New paradigms and challenges. Nat. Rev. Cardiol. 20, 812–829. https://doi.org/10.1038/s41569-023-00887-x (2023).

    Google Scholar 

  4. Murashige, D. et al. Comprehensive quantification of fuel use by the failing and nonfailing human heart. Science 370, 364–368. https://doi.org/10.1126/science.abc8861 (2020).

    Google Scholar 

  5. Zhao, M. et al. Gut bacteria-driven homovanillic acid alleviates depression by modulating synaptic integrity. Cell Metab. https://doi.org/10.1016/j.cmet.2024.03.010 (2024).

    Google Scholar 

  6. De La Haba, G. & Cantoni, G. L. The enzymatic synthesis of S-adenosyl-L-homocysteine from adenosine and homocysteine. J. Biol. Chem. 234, 603–608 (1959).

    Google Scholar 

  7. Fan, M. et al. The association between concentrations of arginine, ornithine, citrulline and major depressive disorder: A meta-analysis. Front Psychiatry 12, 686973. https://doi.org/10.3389/fpsyt.2021.686973 (2021).

    Google Scholar 

  8. Conte, F., van Buuringen, N., Voermans, N. C. & Lefeber, D. J. Galactose in human metabolism, glycosylation and congenital metabolic diseases: Time for a closer look. Biochimica et Biophysica Acta (BBA) - General Subjects 1865, 129898. https://doi.org/10.1016/j.bbagen.2021.129898 (2021).

    Google Scholar 

  9. Chen, R. et al. Transplantation of fecal microbiota rich in short chain fatty acids and butyric acid treat cerebral ischemic stroke by regulating gut microbiota. Pharmacol. Res. 148, 104403. https://doi.org/10.1016/j.phrs.2019.104403 (2019).

    Google Scholar 

  10. Zhang, N. et al. Comprehensive serum metabolic and proteomic characterization on cognitive dysfunction in Parkinson’s disease. Annals Transl. Med. 9, 559. https://doi.org/10.21037/atm-20-4583 (2021).

    Google Scholar 

  11. Spillmann, R. et al. Congenital heart disease in school-aged children: Cognition, education, and participation in leisure activities. Pediatr. Res. 94, 1523–1529. https://doi.org/10.1038/s41390-021-01853-4 (2023).

    Google Scholar 

  12. Dhanasekara, C. S. et al. Association between autism spectrum disorders and cardiometabolic diseases: A systematic review and meta-analysis. JAMA Pediatr. 177, 248–257. https://doi.org/10.1001/jamapediatrics.2022.5629 (2023).

    Google Scholar 

  13. Migdady, I. et al. Brain injury and neurologic outcome in patients undergoing extracorporeal cardiopulmonary resuscitation: A systematic review and meta-analysis. Crit. Care Med. 48, e611–e619. https://doi.org/10.1097/CCM.0000000000004377 (2020).

    Google Scholar 

  14. Hsueh, B. et al. Cardiogenic control of affective behavioural state. Nature 615, 292–299. https://doi.org/10.1038/s41586-023-05748-8 (2023).

    Google Scholar 

  15. von Werdt, L. et al. Stress markers, executive functioning, and resilience among early adolescents with complex congenital heart disease. JAMA Netw. Open 7, e2355373. https://doi.org/10.1001/jamanetworkopen.2023.55373 (2024).

    Google Scholar 

  16. Hou, Y. et al. Rhodiola crenulata alleviates hypobaric hypoxia-induced brain injury by maintaining BBB integrity and balancing energy metabolism dysfunction. Phytomedicine 128, 155529. https://doi.org/10.1016/j.phymed.2024.155529 (2024).

    Google Scholar 

  17. Marasini, S. & Jia, X. Neuroprotective approaches for brain injury after cardiac arrest: Current trends and prospective avenues. J. Stroke 26, 203–230. https://doi.org/10.5853/jos.2023.04329 (2024).

    Google Scholar 

  18. Simats, A., Sager, H. & Liesz, A. Heart brain axis in health and disease: Role of innate and adaptive immunity. Cardiovasc. Res. https://doi.org/10.1093/cvr/cvae185 (2024).

    Google Scholar 

  19. Sandroni, C., Cronberg, T. & Sekhon, M. Brain injury after cardiac arrest: Pathophysiology, treatment, and prognosis. Intensive Care Med. 47, 1393–1414. https://doi.org/10.1007/s00134-021-06548-2 (2021).

    Google Scholar 

  20. Sekhon, M. S., Ainslie, P. N. & Griesdale, D. E. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: A “two-hit” model. Crit. Care 21, 90. https://doi.org/10.1186/s13054-017-1670-9 (2017).

    Google Scholar 

  21. Dridi, H. et al. Heart failure-induced cognitive dysfunction is mediated by intracellular Ca(2+) leak through ryanodine receptor type 2. Nat. Neurosci. 26, 1365–1378. https://doi.org/10.1038/s41593-023-01377-6 (2023).

    Google Scholar 

  22. Huang, W. et al. AHCYL1 senses SAH to inhibit autophagy through interaction with PIK3C3 in an MTORC1-independent manner. Autophagy 18, 309–319. https://doi.org/10.1080/15548627.2021.1924038 (2022).

    Google Scholar 

  23. Shao, M. M. et al. Candidate metabolite markers of peripheral neuropathy in Chinese patients with type 2 diabetes. Am. J. Transl. Res. 14, 5420–5440 (2022).

    Google Scholar 

  24. Zhang, Y. et al. MicroRNA-206 down-regulated human umbilical cord mesenchymal stem cells alleviate cognitive decline in D-galactose-induced aging mice. Cell Death Discov. 8, 304. https://doi.org/10.1038/s41420-022-01097-z (2022).

    Google Scholar 

  25. Zhao, Y. et al. Celecoxib alleviates pathological cardiac hypertrophy and fibrosis via M1-like macrophage infiltration in neonatal mice. iScience 24, 102233. https://doi.org/10.1016/j.isci.2021.102233 (2021).

    Google Scholar 

  26. Zhao, Y., Huang, Z., Gao, L., Ma, H. & Chang, R. Osteopontin/SPP1: A potential mediator between immune cells and vascular calcification. Front. Immunol. 15, 1395596. https://doi.org/10.3389/fimmu.2024.1395596 (2024).

    Google Scholar 

  27. Wang, X., Xu, Z., Chang, R., Zeng, C. & Zhao, Y. High-fructose diet induces cardiac dysfunction via macrophage recruitment in adult mice. J. Cardiovasc. Pharmacol. Ther. 28, 10742484231162249. https://doi.org/10.1177/10742484231162249 (2023).

    Google Scholar 

  28. Nwaiwu, J. et al. Western diet induces mild metabolic impairment and aggravates neuropathology in an experimental mouse model of traumatic brain injury. J. Neurorestoratology https://doi.org/10.1016/j.jnrt.2024.100140 (2024).

    Google Scholar 

  29. Ma, H., Gao, L., Chang, R., Zhai, L. & Zhao, Y. Crosstalk between macrophages and immunometabolism and their potential roles in tissue repair and regeneration. Heliyon 10, e38018. https://doi.org/10.1016/j.heliyon.2024.e38018 (2024).

    Google Scholar 

  30. Huynh, P. et al. Myocardial infarction augments sleep to limit cardiac inflammation and damage. Nature 635, 168–177. https://doi.org/10.1038/s41586-024-08100-w (2024).

    Google Scholar 

  31. Mehla, K. & Singh, P. K. Metabolic regulation of macrophage polarization in cancer. Trends Cancer 5, 822–834. https://doi.org/10.1016/j.trecan.2019.10.007 (2019).

    Google Scholar 

  32. Mouton, A. J. et al. Temporal changes in glucose metabolism reflect polarization in resident and monocyte-derived macrophages after myocardial infarction. Front. Cardiovasc. Med. 10, 1136252. https://doi.org/10.3389/fcvm.2023.1136252 (2023).

    Google Scholar 

  33. Pan, R. Y. et al. Positive feedback regulation of microglial glucose metabolism by histone H4 lysine 12 lactylation in Alzheimer’s disease. Cell Metab. 34, 634-648 e636. https://doi.org/10.1016/j.cmet.2022.02.013 (2022).

    Google Scholar 

  34. Qin, C. et al. Modulation of microglial metabolism facilitates regeneration in demyelination. iScience 26, 106588. https://doi.org/10.1016/j.isci.2023.106588 (2023).

    Google Scholar 

  35. Fang, Z. et al. Whole-body mass spectrometry imaging reveals the systemic metabolic disorder and catecholamines biosynthesis alteration on heart-gut axis in heart failure rat. J. Adv. Res. https://doi.org/10.1016/j.jare.2024.09.001 (2024).

    Google Scholar 

  36. Boyle, S. H. et al. Metabolomics analysis reveals insights into biochemical mechanisms of mental stress-induced left ventricular dysfunction. Metabolomics 11, 571–582. https://doi.org/10.1007/s11306-014-0718-y (2015).

    Google Scholar 

  37. Osse, R. J. et al. High preoperative plasma neopterin predicts delirium after cardiac surgery in older adults. J. Am. Geriatr. Soc. 60, 661–668. https://doi.org/10.1111/j.1532-5415.2011.03885.x (2012).

    Google Scholar 

  38. Menaker, Y. et al. Stratification of atherosclerosis based on plasma metabolic states. J. Clin. Endocrinol. Metab. 109, 1250–1262. https://doi.org/10.1210/clinem/dgad672 (2024).

    Google Scholar 

  39. Bonifacic, D. et al. Values of vanillylmandelic acid and homovanillic acid in the urine as potential prognostic biomarkers in ischaemic stroke patients. Biomarkers 22, 790–797. https://doi.org/10.1080/1354750X.2017.1351001 (2017).

    Google Scholar 

  40. Milliez, P. et al. Effects of spironolactone alone and in addition to a beta-blocker on myocardial histological and electrical remodeling in chronic severe failing rat hearts. J. Cardiovasc. Pharmacol. 60, 315–321. https://doi.org/10.1097/FJC.0b013e318260e688 (2012).

    Google Scholar 

  41. Rao, Y., Bai, Y., Li, X., Du, B. & Peng, B. The evolution of microglia replacement: A new paradigm for CNS disease therapy. Cell Stem Cell 32, 1807–1832. https://doi.org/10.1016/j.stem.2025.10.014 (2025).

    Google Scholar 

  42. Li, Y. et al. Targeting formyl peptide receptor 1 reduces brain inflammation and neurodegeneration. Science 390, eadq1177. https://doi.org/10.1126/science.adq1177 (2025).

    Google Scholar 

  43. Liu, J., Zaidi, A. & Pike, C. J. Microglia/macrophage-specific deletion of TLR-4 protects against neural effects of diet-induced obesity in a sexually dimorphic manner. J. Neuroinflammation 22, 214. https://doi.org/10.1186/s12974-025-03534-z (2025).

    Google Scholar 

  44. Wang, S. et al. HK2 in microglia and macrophages contribute to the development of neuropathic pain. Glia 72, 396–410. https://doi.org/10.1002/glia.24482 (2024).

    Google Scholar 

  45. Kokkosis, A. G. et al. Chronic psychosocial stress triggers microglial-/macrophage-induced inflammatory responses leading to neuronal dysfunction and depressive-related behavior. Glia 72, 111–132. https://doi.org/10.1002/glia.24464 (2024).

    Google Scholar 

  46. Farhangian, M., Azarafrouz, F., Chavoshinezhad, S. & Dargahi, L. Intranasal interferon-beta alleviates anxiety and depressive-like behaviors by modulating microglia polarization in an Alzheimer’s disease model. Neurosci. Lett. 792, 136968. https://doi.org/10.1016/j.neulet.2022.136968 (2023).

    Google Scholar 

  47. Zhao, Y., Chang, R. & Zeng, C. Protocol for cryoinjury model in neonatal mice for heart regeneration and repair research. STAR Protoc. 2, 100623. https://doi.org/10.1016/j.xpro.2021.100623 (2021).

    Google Scholar 

  48. du Sert, N. P. et al. The ARRIVE guidelines 2.0: Updated guidelines for reporting animal research. BMJ. Open Sci. 4, e100115. https://doi.org/10.1136/bmjos-2020-100115 (2020).

    Google Scholar 

  49. Xie, G. et al. A metabolite array technology for precision medicine. Anal. Chem. 93, 5709–5717. https://doi.org/10.1021/acs.analchem.0c04686 (2021).

    Google Scholar 

  50. Bornstein, M. R., Tian, R. & Arany, Z. Human cardiac metabolism. Cell Metab. 36, 1456–1481. https://doi.org/10.1016/j.cmet.2024.06.003 (2024).

    Google Scholar 

  51. Sun, Q., Karwi, Q. G., Wong, N. & Lopaschuk, G. D. Advances in myocardial energy metabolism: Metabolic remodelling in heart failure and beyond. Cardiovasc. Res. 120, 1996–2016. https://doi.org/10.1093/cvr/cvae231 (2024).

    Google Scholar 

  52. Ji, X. et al. Sphingolipid metabolism controls mammalian heart regeneration. Cell Metab. 36, 839-856 e838. https://doi.org/10.1016/j.cmet.2024.01.017 (2024).

    Google Scholar 

  53. Zhou, Q. F. et al. Tyrosine to threonine ratio was related to heart failure with reduced or mildly reduced ejection fraction. ESC Heart Fail. 11, 1567–1579. https://doi.org/10.1002/ehf2.14700 (2024).

    Google Scholar 

  54. Petersson, J. N. et al. Unraveling metabolic changes following stroke: Insights from a urinary metabolomics analysis. Metabolites https://doi.org/10.3390/metabo14030145 (2024).

    Google Scholar 

  55. Tong, S. Y. et al. Serum glial cell line-derived neurotrophic factor (GDNF) a potential biomarker of executive function in Parkinson’s disease. Front. Neurosci. 17, 1136499. https://doi.org/10.3389/fnins.2023.1136499 (2023).

    Google Scholar 

  56. Wieselgren, I. M. & Lindstrom, L. H. CSF levels of HVA and 5-HIAA in drug-free schizophrenic patients and healthy controls: A prospective study focused on their predictive value for outcome in schizophrenia. Psychiatry Res. 81, 101–110. https://doi.org/10.1016/s0165-1781(98)00090-0 (1998).

    Google Scholar 

  57. Yadav, D. K., Chang, A. C., Grooms, N. W. F., Chung, S. H. & Gabel, C. V. O-GlcNAc signaling increases neuron regeneration through one-carbon metabolism in Caenorhabditis elegans. Elife https://doi.org/10.7554/eLife.86478 (2024).

    Google Scholar 

  58. Fernandes, C. et al. Pyomelanin synthesis in Alternaria alternata inhibits DHN-melanin synthesis and decreases cell wall chitin content and thickness. Front. Microbiol. 12, 691433. https://doi.org/10.3389/fmicb.2021.691433 (2021).

    Google Scholar 

  59. Wang, Z. et al. Metabolic reprogramming in skin wound healing. Burns Trauma 12, tkad047. https://doi.org/10.1093/burnst/tkad047 (2024).

    Google Scholar 

  60. Zhou, W. et al. SENP1-Sirt3 signaling promotes alpha-ketoglutarate production during M2 macrophage polarization. Cell Rep. 39, 110660. https://doi.org/10.1016/j.celrep.2022.110660 (2022).

    Google Scholar 

  61. Kerr, S. J. Competing methyltransferase systems. J. Biol. Chem. 247, 4248–4252 (1972).

    Google Scholar 

  62. Wang, J. N. et al. Inhibition of METTL3 attenuates renal injury and inflammation by alleviating TAB3 m6A modifications via IGF2BP2-dependent mechanisms. Sci. Transl. Med. 14, eabk2709. https://doi.org/10.1126/scitranslmed.abk2709 (2022).

    Google Scholar 

  63. Yan, P. et al. Crosstalk of Synapsin1 palmitoylation and phosphorylation controls the dynamicity of synaptic vesicles in neurons. Cell Death Dis. 13, 786. https://doi.org/10.1038/s41419-022-05235-4 (2022).

    Google Scholar 

  64. Zhang, T. & Brown, J. H. Role of Ca2+/calmodulin-dependent protein kinase II in cardiac hypertrophy and heart failure. Cardiovasc. Res. 63, 476–486. https://doi.org/10.1016/j.cardiores.2004.04.026 (2004).

    Google Scholar 

  65. Yang, T., Wu, X. & Wang, X. HMGB1 regulates autophagy via TLR4/NF-κB signaling pathway in myocardial injury induced by coronary microembolization. Eur. J. Med. Res. 30(1), 943. https://doi.org/10.1186/s40001-025-03220-z (2025).

    Google Scholar 

  66. Kopin, I. J., White, J. H. & Bankiewicz, K. A new approach to biochemical evaluation of brain dopamine metabolism. Cell. Mol. Neurobiol. 8, 171–179. https://doi.org/10.1007/BF00711243 (1988).

    Google Scholar 

  67. Stefani, A. et al. Homovanillic acid in CSF of mild stage Parkinson’s disease patients correlates with motor impairment. Neurochem. Int. 105, 58–63. https://doi.org/10.1016/j.neuint.2017.01.007 (2017).

    Google Scholar 

  68. Gatarek, P. et al. The determination of Trimethylamine N-Oxide and organic acids connected with gut microbiota in the urine of Parkinson’s disease patients: A pilot study. Int. J. Mol. Sci. https://doi.org/10.3390/ijms26104575 (2025).

    Google Scholar 

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Funding

This work was supported by the Guangdong Medical Research Foundation, China (Grant number A2024454), the Scientific Research Projects of Medical and Health Institutions of Longhua District, Shenzhen, China (Grant number 2023003, 2023036, 2023074), Heyuan City Foundation of Science and Technology (Grant number: 211228101470423) and Guangdong Medical Science Foundation (Grant number: B2022164).

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Author notes

  1. Zhenfei Wu, Zujuan Huang, Fengpei Ding, and Yanli Zhao have contributed equally to this work and share first authorship.

Authors and Affiliations

  1. Department of Cardiovascular Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, China

    Zhenfei Wu, Zujuan Huang, Fengpei Ding, Changchun Zeng, Rong Chang & Yanli Zhao

  2. School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China

    Hongbo Ma

  3. Department of Clinical Laboratory, Shenzhen Longhua District Central Hospital, Shenzhen, China

    Wenbin Kuang

  4. Department of Nursing, Heyuan People’s Hospital, Heyuan, 517000, Guangdong, China

    Chuntao Deng

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Contributions

Z.W., Z.H., F.D., H.M., C.D., W.K., and Y.Z. performed experiments and analyzed the data, Z.W., Z.H., R.C., C.Z.,C.D., W.K., and Y.Z. provided chemical reagents and experimental machines; Y.Z designed, wrote and corrected the manuscript.

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Correspondence to Wenbin Kuang or Yanli Zhao.

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Wu, Z., Huang, Z., Ding, F. et al. Homovanillic acid improves anxiety by regulating F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury. Sci Rep (2026). https://doi.org/10.1038/s41598-026-43510-y

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  • Received: 03 October 2025

  • Accepted: 04 March 2026

  • Published: 18 March 2026

  • DOI: https://doi.org/10.1038/s41598-026-43510-y

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Keywords

  • Homovanillic acid
  • F4/80+ microglia/macrophage
  • Neonatal cardiac injury
  • Behavioral symptoms
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