Preview

Clinical Medicine (Russian Journal)

Advanced search
Open Access Open Access  Restricted Access Subscription Access

Endothelial dysfunction in pathogenesis of immunoinflammatory diseases and comorbidites

https://doi.org/10.30629/0023-2149-2024-102-11-12-868-873

Abstract

Currently, rheumatic diseases are classified as a group of immune-inflammatory disorders, in which endothelial dysfunction plays a significant role in their pathogenesis. The aim of the study was to present the heterogeneous pathogenesis of immune inflammation, to trace the links of pathogenesis, and to highlight the role of endothelial dysfunction in immune-inflammatory rheumatic diseases.

Material and methods. A total of 144 patients were examined: 80 with rheumatoid arthritis (RA) and 64 with systemic lupus erythematosus (SLE). The study involved the determination of rheumatoid factor (RF) IgG, C-reactive protein (CRP), soluble vascular cell adhesion molecule (sVCAM-1), von Willebrand factor antigen (vWF Ag), endothelin-1 (ET-1), and the number of desquamated endothelial cells (DEC) counted using a Goryaev chamber.

Results. Signs of endothelial dysfunction were identified in patients with RA and SLE, as evidenced by significant differences in endothelial activation markers compared to the control group. The level of ET-1 was lower in patients with RA at 2.54 [0.09; 3.51] fmol/ ml, compared to 5.96 [0.20; 9.54] fmol/ml in patients with SLE, and 0.46 [0.34; 0.56] fmol/ml in the control group, p < 0.05. The level of sVCAM-1 in RA was 1929 [1297.6; 2739.6] ng/ml, in the SLE group it was 1497.3 [919.6; 2348.6] ng/ml, and in the control group it was 750 [250; 890] ng/ml, p < 0.01. The number of DEC was significantly higher. An increase in IL-8 levels was noted in the RA group at 414.2 [285; 541] pg/ml, in the SLE group at 335.2 [280; 398.6] pg/ml, and in the control group at 208 [206; 211] pg/ml, p < 0.01. There was an increase in CRP levels in RA up to 19.67 [4.2; 27] mg/l, and in SLE up to 16.5 [10; 22], which significantly exceeded the control group value of 2.6 [2.2; 3.3], p < 0.01. In patients with RA and SLE, markers of endothelial activation positively correlated with the level of RF IgG and indicators of immune inflammation: with increasing values of CRP and ESR, rising concentrations of sVCAM-1, vWF Ag, and the number of DEC, p < 0.01.

Conclusion. Endothelial dysfunction plays a significant role in the pathogenesis of rheumatic diseases, and its correction may lead to the development of new therapeutic targets and help prevent complications in this patient category.

About the Authors

N. P. Shilkina
Yaroslavl State Medical University
Russian Federation

Nataliya P. Shilkina — Doctor of Medical Sciences, Professor of the Department of Propaedeutics of Internal Diseases

Yaroslavl



I. E. Yunonin
Yaroslavl State Medical University
Russian Federation

Igor E. Yunonin — Candidate of Medical Sciences, Associate Professor of the Department of Propaedeutics of Internal Diseases

Yaroslavl



I. V. Dryazhenkova
Yaroslavl State Medical University
Russian Federation

Irina V. Dryazhenkova — Doctor of Medical Sciences, Associate Professor of the Department of Hygiene

Yaroslavl



S. V. Butusova
Central City Clinical Hospital
Russian Federation

Svetlana V. Butusova — Candidate of Medical Sciences, Head of polyclinic No. 1

Yaroslavl



M. V. Ilyin
Yaroslavl State Medical University
Russian Federation

Mikhail V. Ilyin — Doctor of Medical Sciences, Associate Professor, Head of the Department of Therapy named after Professor E.N. Dormidontov

Yaroslavl



J. E. Chetvertakova
Yaroslavl State Medical University
Russian Federation

Zhanna E. Chetvertakova — Candidate of Medical Sciences, Assistant Professor at the Department of Propaedeutics of Internal Diseases

Yaroslavl



References

1. Nasonov E.L., Eliseev M.S. Role of interleukin 1 in the development of human diseases. Rheumatology science and practice. 2016 ;54(1):60–77. (In Russian). DOI: 10.14412/1995-4484-2016-60-77

2. Nasonov E.L., Reshetniak T.M., Alekberova Z.S. Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity. Therapeutic archive. 2020;92(5):4–14. (In Russian). DOI: 10.26442/00403660.2020.05.000697

3. Nasonov E.L. 2019 Coronavirus disease (COVID-19): contribution of rheumatology. Terapevticheskii arkhiv. 2021;93(5):537–550. (In Russian). DOI: 10.26442/00403660.2021.05.200799

4. Harrison D.G. Cellular and molecular mechanisms of endothelial cell dysfunction. J. Clin. Investig. 1997;100:2153–2157. DOI: 10.14412/1995-4484-2016-60-77

5. Quick S., Moss J., Rajani R.M. et al. Vessel for change: endothelial dysfunction in cerebral small vessel disease. Trends Neurosci. 2021;44:289–305.

6. Silverman M.D., Haas C.S., Rad A.M. et al. The role of vascular cell adhesion molecule 1/very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium. Arthritis Rheum. 2007;56:1817–1826.

7. Klimiuk P., Sierakowski S., Latosiewicz R. et al. Soluble adhesion molecules (ICAM-1, VCAM-1, and E-selectin) and vascular endothelial growth factor (VEGF) in patients with distinct variants of rheumatoid synovitis. Ann. Rheum. Dis. 2002;61:804–809.

8. Salem H.R., Zahran E.S. Vascular cell adhesion molecule-1 in rheumatoid arthritis patients: Relation to disease activity, oxidative stress, and systemic inflammation. Saudi Med. J. 2021; 42(6):620– 628. DOI: 10.15537/smj.2021.42.6.20200753

9. Maiuolo J., Muscoli C., Gliozzi M. et al. Endothelial dysfunction and extra-articular neurological manifestations in rheumatoid arthritis. Biomolecules. 2021;11:81.

10. Poveshchenko OV, Poveshchenko AF, Konenkov VI Endothelial progenitornye cells and neovaskulogenez. Successes of contemporary biology. 2012;132(1):69–76. (In Russian).

11. Komici K., Perna A., Rocca A. et al. Endothelial progenitor cells and rheumatoid arthritis: response to endothelial dysfunction and clinical evidences. Int. J. Mol. Sci. 2021;22(24):13675. DOI: 10.3390/ijms222413675

12. Akhmedov A., Crucet M., Simic B. et al. TNFα induces endothelial dysfunction in rheumatoid arthritis via LOX-1 and arginase 2: reversal by monoclonal TNFα antibodies. Cardiovasc. Res. 2022;118(1):254–266. DOI: 10.1093/cvr/cvab005

13. Anyfanti P, Gavriilaki E , Douma S. et al. Endothelial dysfunction in patients with rheumatoid arthritis: the role of hypertension. Curr. Hypertens. Rep. 2020;22(8):56. DOI: 10.1007/s11906-020-01064-y

14. Anselm M., Jerry K., Yen Chan. Endothelial function and endothelial progenitor cells in systemic lupus erythematosus. Nat. Rev. Rheumatol. 2022;18(5):286–300. DOI: 10.1038/s41584-022-00770-y

15. Yada N., Yoshimoto K., Kawashima H. et al. Plasma level of von Willebrand factor propeptide at diagnosis: a marker of subsequent renal dysfunction in autoimmune rheumatic diseases. Clin. Appl. Thromb. Hemost. 2020 Jan-Dec. DOI: 26:1076029620938874

16. Mancardi D., Arrigo E., Cozzi M. et al. Endothelial dysfunction and cardiovascular risk in lupus nephritis: New roles for old players? Eur. J. Clin. Invest. 2021;51(2):e13441. DOI: 10.1111/eci.13441

17. McClung D.M., Kalusche W.J., Joneset K.E. et al. Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus. Physiol. Rep. 2021;9(3):e14734. DOI: 10.14814/phy2.14734

18. Khirmanov V.N. COVID-19 as systemic disease. Clinicheskaya Pharmacologiya and Therapiya. 2021;30(1):5–15. (In Russian). DOI: 10.14412/1995-4484-2016-60-77

19. Becker R.C. Editorial. COVID19associated vasculitis and vasculopathy. J. Thrombosis and Thrombolysis. 2020;50:499–511. DOI: 10.32756/0869-5490-2021-1-5-15


Review

For citations:


Shilkina N.P., Yunonin I.E., Dryazhenkova I.V., Butusova S.V., Ilyin M.V., Chetvertakova J.E. Endothelial dysfunction in pathogenesis of immunoinflammatory diseases and comorbidites. Clinical Medicine (Russian Journal). 2024;102(11-12):868-873. (In Russ.) https://doi.org/10.30629/0023-2149-2024-102-11-12-868-873

Views: 162


ISSN 0023-2149 (Print)
ISSN 2412-1339 (Online)