ABSTRACT
Purpose: The field of osteoarthritis (OA) biology is rapidly evolving and brilliant progress has been made this year as well. Methods: Landmark studies of OA biology published in 2021 and early 2022 were selected through PubMed searches and classified by their molecular mechanisms, and it was largely divided into the intra-cellular mechanisms and the inter-compartment or inter-cellular interaction in OA progression. Results: The intra-cellular mechanisms involving OA progression included 1) Piezo1/TRPV4-mediated calcium signaling, 2) low grade inflammation by TLR-CD14-LBP complex and IKKβ-NFkB signaling, 3) PGRN/TNFR2/14-3-3ε/Elk-1 anabolic cascade, 4) G protein-coupled receptor (GPCR) signaling, 5) mechanical loading-cilia/Ift88-hedgehog signaling, 6) mitochondrial fission by ERK1/2-DRP1 pathway, and 7) hypoxia-DOT1L-H3K79 methylation pathway. The studies on inter-compartment or inter-cellular interaction in OA progression included the following subjects: 1) the anabolic role of Lubricin, a proteoglycan from superficial zone cells, 2) osteoclast-chondrocyte interaction via exosomal miRNA and sphingosine 1-phosphate (S1P), 3) αV integrin-mediated TGFβ activation by mechanical loading, 4) TGFβ-mediated suppression of sclerostin in osteocytes, 5) catabolic role of Flightless I as a DAMPs-triggering molecule, and 6) catabolic role of paracrine signaling from fat. Conclusions: Despite the disastrous Covid-19 pandemic situation, many outstanding studies have expanded the boundary of OA biology. They give us not only critical insight on pathophysiology, but also clue for the treatment of OA.
ABSTRACT
The proceedings contain 34 papers. The topics discussed include: combinatorial maturation of patient stem cell-derived atrial cardiomyocytes unmasks mechanism of atrial fibrillation induced by NPPA gene mutation;the pathogenesis of Covid-19 myocardial injury: an immunohistochemical study of postmortem biopsies;mitochondrial optogenetic-mediated preconditioning protects cardiomyocytes from stress-induced injury;the aldose reductase inhibitor At-001 improves cardiac efficiency and decreases diastolic dysfunction in an animal model of diabetic cardiomyopathy: comparative and add-on studies versus SGLT-2 inhibition;cardiomyocyte specific deletion Of Trpv4 offers cardio-protection independent of cardiac fibrosis following pressure overload-induced hypertrophy;and sacubitril-valsartan protects against aortic aneurysm progression via regulating neprilysin-induced vascular smooth muscle cell apoptosis.