Systemic sclerosis (SSc) is a complex autoimmune disease characterized by significant fibrosis of the skin and internal organs, with the main involvement of the lungs, kidneys, heart, esophagus, and intestines. SSc is also characterized by macro- and microvascular damage with reduced peripheral blood perfusion. Several studies have reported more than 240 pathways and numerous dysregulation proteins, giving insight into how the field of biomarkers in SSc is still extremely complex and evolving. Antinuclear antibodies (ANA) are present in more than 90% of SSc patients, and anti-centromere and anti-topoisomerase I antibodies are considered classic biomarkers with precise clinical features. Recent studies have reported that trans-forming growth factor β (TGF-β) plays a central role in the fibrotic process. In addition, interferon regulatory factor 5 (IRF5), interleukin receptor-associated kinase-1 (IRAK-1), connective tissue growth factor (CTGF), transducer and activator of transcription signal 4 (STAT4), pyrin-containing domain 1 (NLRP1), as well as genetic factors, including DRB1 alleles, are implicated in SSc damage. Several interleukins (e.g., IL-1, IL-6, IL-10, IL-17, IL-22, and IL-35) and chemokines (e.g., CCL 2, 5, 23, and CXC 9, 10, 16) are elevated in SSc. While adiponectin and maresin 1 are reduced in patients with SSc, biomarkers are important in research but will be increasingly so in the diagnosis and therapeutic approach to SSc. This review aims to present and highlight the various biomarker molecules, pathways, and receptors involved in the pathology of SSc.
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http://dx.doi.org/10.3390/cimb45100490 | DOI Listing |
J Shoulder Elbow Surg
December 2024
Orthopedic Biomechanics Laboratory, Congress Medical Foundation, Pasadena, CA, USA. Electronic address:
Background: The restriction of active internal rotation (IR) after reverse shoulder arthroplasty (RSA) poses a challenging problem for reconstructive shoulder surgeons, particularly in patients suffering from massive rotator cuff tears (mRCT) with subscapularis (SSC) deficiency. This study aims to evaluate the biomechanical effectiveness of different tendon transfer techniques following medialized glenoid and lateralized humerus RSA in improving internal rotation (IR) strength.
Methods: Eight cadaveric shoulder specimens were evaluated using a custom shoulder testing system designed to simulate loading conditions typical of mRCT with SSC insufficiency.
Adv Rheumatol
December 2024
Department of Immunology & Molecular Medicine, Sher-I-Kashmir Institute of Medical Sciences (SKIMS), Soura, Srinagar, Jammu and Kashmir, 190011, India.
Background: As a master immune system regulator, transforming growth factor β1 (TGF-β1) is closely linked to the complicated pathophysiology and development of systemic sclerosis (SSc), a multisystem fibrotic disease.
Objective: We aim to evaluate the transcriptional levels of TGF-β1 mRNA in PBMCs, assess the TGF-β1 serum levels of SSc patients, and compare them with those of healthy subjects.
Methods: PBMCs were isolated from whole blood of 50 SSc patients and in 30 healthy controls.
Mol Med
December 2024
Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, P.R. China.
Background: ADAM19 (ADAM Metallopeptidase Domain 19) is known to be involved in extracellular matrix (ECM) remodeling, yet its specific function in systemic sclerosis (SSc) fibrosis remains unclear.
Objectives: This study sought to clarify the role and underlying mechanism of ADAM19 in SSc skin fibrosis.
Methods: The expression of ADAM19 was assessed in skin tissues of SSc and wound healing using publicly available transcriptome datasets.
Clin Exp Rheumatol
December 2024
Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Objectives: Systemic sclerosis (SSc), a chronic autoimmune disorder, characterised by local inflammation and progressive fibrosis. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) has been established as a key mediator in fibrotic processes across multiple organs, primarily through binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the precise role of the TWEAK/Fn14 signalling in SSc pathogenesis remains unclear.
View Article and Find Full Text PDFFront Med (Lausanne)
December 2024
Department of Health Sciences, University of Florence, Florence, Italy.
Objectives: (a) Assessing mental disorders, psychological distress, psychological wellbeing in patients with systemic sclerosis (SSc); (b) identifying psychological features independently contributing to the status of having the diagnosis of SSc.
Methods: Two hundred SSc outpatients were compared with 100 healthy subjects. Mental disorders were assessed via the Mini International Neuropsychiatric Interview (MINI).
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