Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic, persistent autoimmune disease that causes severe joint tissue damage and irreversible disability. Cumulative evidence suggests that patients suffering from RA for long durations are at risk of functional damage to cardiovascular, kidney, lung, and other tissue...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
|
| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2022/2280973 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832561776983539712 |
|---|---|
| author | Qianlei Wang James Asenso Ning Xiao Jinzhang Gao Feng Xiao Jiajie Kuai Wei Wei Chun Wang |
| author_facet | Qianlei Wang James Asenso Ning Xiao Jinzhang Gao Feng Xiao Jiajie Kuai Wei Wei Chun Wang |
| author_sort | Qianlei Wang |
| collection | DOAJ |
| description | Rheumatoid arthritis (RA) is a chronic, persistent autoimmune disease that causes severe joint tissue damage and irreversible disability. Cumulative evidence suggests that patients suffering from RA for long durations are at risk of functional damage to cardiovascular, kidney, lung, and other tissues. This seriously affects the quality of work and life of patients. To date, no clear etiology of RA has been found. Recent studies have revealed that the massive proliferation of synoviocytes and immune cells requires a large amount of energy supply. Rapid energy supply depends on the anaerobic glucose metabolic pathway in both RA animal models and clinical patients. Anaerobic glycolysis can increase intracellular lactic acid (LA) content. LA induces the overexpression of monocarboxylate transporters (MCTs) in cell membranes. MCTs rapidly transport LA from the intracellular to the intercellular or articular cavity. Hence, a relatively high accumulation of LA could be formed in the intercellular and articular cavities of inflammatory joints. Moreover, LA contributes to the migration and activation of immune cells. Immune cells proliferate and secrete interleukins (IL) including IL-1, IL-2, IL-13, IL-17, and other inflammatory factors. These inflammatory factors enhance the immune inflammatory response of the body and aggravate the condition of RA patients. In this paper, the effects of LA on RA pathogenesis will be summarized from the perspective of the production, transport, and metabolism of synoviocytes and immune cells. Additionally, the drugs involved in the production, transport, and metabolism of LA are highlighted. |
| format | Article |
| id | doaj-art-809d053300274d619ffba4f7e4ec3d59 |
| institution | Kabale University |
| issn | 2314-7156 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-809d053300274d619ffba4f7e4ec3d592025-02-03T01:24:10ZengWileyJournal of Immunology Research2314-71562022-01-01202210.1155/2022/2280973Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid ArthritisQianlei Wang0James Asenso1Ning Xiao2Jinzhang Gao3Feng Xiao4Jiajie Kuai5Wei Wei6Chun Wang7Institute of Clinical PharmacologyDepartment of Pharmaceutical SciencesInstitute of Clinical PharmacologyInstitute of Clinical PharmacologyInstitute of Clinical PharmacologyInstitute of Clinical PharmacologyInstitute of Clinical PharmacologyInstitute of Clinical PharmacologyRheumatoid arthritis (RA) is a chronic, persistent autoimmune disease that causes severe joint tissue damage and irreversible disability. Cumulative evidence suggests that patients suffering from RA for long durations are at risk of functional damage to cardiovascular, kidney, lung, and other tissues. This seriously affects the quality of work and life of patients. To date, no clear etiology of RA has been found. Recent studies have revealed that the massive proliferation of synoviocytes and immune cells requires a large amount of energy supply. Rapid energy supply depends on the anaerobic glucose metabolic pathway in both RA animal models and clinical patients. Anaerobic glycolysis can increase intracellular lactic acid (LA) content. LA induces the overexpression of monocarboxylate transporters (MCTs) in cell membranes. MCTs rapidly transport LA from the intracellular to the intercellular or articular cavity. Hence, a relatively high accumulation of LA could be formed in the intercellular and articular cavities of inflammatory joints. Moreover, LA contributes to the migration and activation of immune cells. Immune cells proliferate and secrete interleukins (IL) including IL-1, IL-2, IL-13, IL-17, and other inflammatory factors. These inflammatory factors enhance the immune inflammatory response of the body and aggravate the condition of RA patients. In this paper, the effects of LA on RA pathogenesis will be summarized from the perspective of the production, transport, and metabolism of synoviocytes and immune cells. Additionally, the drugs involved in the production, transport, and metabolism of LA are highlighted.http://dx.doi.org/10.1155/2022/2280973 |
| spellingShingle | Qianlei Wang James Asenso Ning Xiao Jinzhang Gao Feng Xiao Jiajie Kuai Wei Wei Chun Wang Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis Journal of Immunology Research |
| title | Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis |
| title_full | Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis |
| title_fullStr | Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis |
| title_full_unstemmed | Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis |
| title_short | Lactic Acid Regulation: A Potential Therapeutic Option in Rheumatoid Arthritis |
| title_sort | lactic acid regulation a potential therapeutic option in rheumatoid arthritis |
| url | http://dx.doi.org/10.1155/2022/2280973 |
| work_keys_str_mv | AT qianleiwang lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT jamesasenso lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT ningxiao lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT jinzhanggao lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT fengxiao lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT jiajiekuai lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT weiwei lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis AT chunwang lacticacidregulationapotentialtherapeuticoptioninrheumatoidarthritis |