Anti‐mitochondrial antibodies in Indian patients with idiopathic inflammatory myopathies

Gaur, Prithvi Sanjeevkumar; Naveen, R; Anuja, Anamika Kumari; Singh, Mantabya; Kumar, Mandhir; Muhammed, Rizwan; Sahu, Ankit Kumar; Agarwal, Vikas; Gupta, Latika

doi:10.1111/1756-185x.14320

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…Mitochondrial abnormalities in juvenile DM patients with CC include increased levels of cell-free mitochondrial DNA (mtDNA) in serum and the presence of anti-mitochondrial antibodies (AMA) (Table 1) [68,76]. In electron microscopy, intramitochondrial calcification was associated with degenerate muscle fibers and mitochondrial extrusion [68].…”

Section: Dermatomyositismentioning

confidence: 99%

Innate Immunity in Calcinosis Cutis

Jiang

Petty

Nicholas

2022

Immuno

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Calcinosis cutis is the deposition of calcium salts in the skin and subcutaneous tissue, manifesting as variably shaped papules, nodules, and plaques that can substantially impair quality of life. The pathophysiology of calcinosis cutis involves dysregulation of proinflammatory cytokines, leukocytes, and other components of the innate immune system. In some conditions associated with calcinosis cutis, elevated serum calcium, phosphate, and vitamin D may also perturb innate immunity. The mechanisms by which these lead to cutaneous and subcutaneous calcification likely parallel those seen in vascular calcification. The role of aberrant innate immunity is further supported by the association between various autoantibodies with calcinosis cutis, such as anti-MDA5, anti-NXP2, anti-centromere, and anti-topoisomerase I. Treatments for calcinosis cutis remain limited and largely experimental, although mechanistically many therapies appear to focus on dampening innate immune responses. Further research is needed to better understand the innate immune pathophysiology and establish treatment options based on randomized-controlled trials.

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Section: Dermatomyositismentioning

confidence: 99%