1 258 76 ADVANCES IN PATHOGENESIS AND NANOPARTICLES (NPS)-MEDIATED TREATMENT OF PSORIASIS. PSORIASIS IS A CHRONIC PAPULOSQUAMOUS SKIN DISEASE WITH AN AUTOIMMUNE PATHOGENIC TRAITS AND STRONG GENETIC PREDISPOSITION. IN THE PAST FEW DECADES, WITH THE RAPID DEVELOPMENT OF MOLECULAR BIOLOGY AND CELL BIOLOGY, THE INHERENT PATHOGENESIS OF PSORIASIS HAS BEEN GRADUALLY ELUCIDATED, IN WHICH CYTOKINE INFLAMMATORY LOOPS, CELL SIGNALING PATHWAYS, AND EPIGENETIC FACTORS SUCH AS MIRNAS HAVE BEEN DEMONSTRATED TO PLAY IMPORTANT ROLES IN REGULATING THE DEVELOPMENT AND PROGRESSION OF PSORIASIS. MORE IMPORTANTLY, UNDERSTANDING THE PATHOGENESIS OF PSORIASIS HAS PROMOTED THE DEVELOPMENT OF EFFECTIVE TREATMENT FOR PSORIASIS. IN THIS REVIEW, WE SYSTEMICALLY SUMMARIZED THE MOLECULAR MECHANISMS REGULATING THE DEVELOPMENT AND PROGRESSION PSORIASIS, INTRODUCED VARIOUS THERAPEUTICS USED FOR CLINICAL PSORIASIS THERAPY, AND HIGHLIGHTED THE RECENT ADVANCES IN NANOPARTICLES (NPS)-MEDIATED DRUG DELIVERY FOR PSORIASIS TREATMENT. 2022 2 6276 31 THE PATHOGENIC ROLE OF DYSREGULATED EPIGENETIC MODIFICATIONS IN AUTOIMMUNE DISEASES. AUTOIMMUNE DISEASES CAN BE CHRONIC WITH RELAPSE OF INFLAMMATORY SYMPTOMS, BUT IT CAN BE ALSO ACUTE AND LIFE-THREATENING IF IMMUNE CELLS DESTROY LIFE-SUPPORTING ORGANS, SUCH AS LUPUS NEPHRITIS. THE ETIOPATHOGENESIS OF AUTOIMMUNE DISEASES HAS BEEN REVEALED AS THAT GENETICS AND ENVIRONMENTAL FACTORS-MEDIATED DYSREGULATED IMMUNE RESPONSES CONTRIBUTE TO THE INITIATION AND DEVELOPMENT OF AUTOIMMUNE DISORDERS. HOWEVER, THE CURRENT UNDERSTANDING OF PATHOGENESIS IS LIMITED AND THE UNDERLYING MECHANISM HAS NOT BEEN WELL DEFINED, WHICH LOWS THE DEVELOPMENT OF NOVEL BIOMARKERS AND NEW THERAPEUTIC STRATEGIES FOR AUTOIMMUNE DISEASES. TO IMPROVE THIS, BROADENING AND DEEPENING OUR UNDERSTANDING OF PATHOGENESIS IS AN UNMET NEED. AS GENETIC SUSCEPTIBILITY CANNOT EXPLAIN THE LOW ACCORDANCE RATE OF INCIDENCE IN HOMOZYGOUS TWINS, EPIGENETIC REGULATIONS MIGHT BE AN ADDITIONAL EXPLANATION. THEREFORE, THIS REVIEW WILL SUMMARIZE CURRENT PROGRESS OF STUDIES ON EPIGENETIC DYSREGULATIONS CONTRIBUTING TO AUTOIMMUNE DISEASES, INCLUDING SLE, RHEUMATOID ARTHRITIS (RA), PSORIASIS, TYPE 1 DIABETES (T1D), AND SYSTEMIC SCLEROSIS (SSC), HOPEFULLY PROVIDING OPINIONS ON ORIENTATION OF FUTURE RESEARCH, AS WELL AS DISCUSSING THE CLINICAL UTILIZATION OF POTENTIAL BIOMARKERS AND THERAPEUTIC STRATEGIES FOR THESE DISEASES. 2019 3 6649 21 UPDATE ON ENDOMETRIOSIS PATHOGENESIS. ENDOMETRIOSIS IS A CHRONIC, INFLAMMATORY, CONDITION OF HIGH INCIDENCE AND SERIOUS REPRODUCTIVE AND GENERAL HEALTH CONSEQUENCES. UNDERSTANDING THE PATHOGENESIS OF ENDOMETRIOSIS IS CRUCIAL FOR PROPER DIAGNOSTIC AND ORDERING THE MOST EFFECTIVE TREATMENT. EVEN THOUGH THERE IS A LARGE BODY OF DATA REGARDING THIS PATHOLOGY OUR UNDERSTANDING OF THE PATHOGENESIS OF THIS DISEASE REMAINS INCOMPLETE. THE AIM OF THIS REVIEW IS TO SUMMARIZE CONTEMPORARY DATA REGARDING PATHOGENESIS OF ENDOMETRIOSIS. CURRENT DATA REGARDING ENDOMETRIAL ORIGIN, METAPLASTIC AND MULLERIAN EMBRYONIC RESTS THEORY WILL BE REVIEWED HERE. ALSO GENETIC, EPIGENETIC, ENVIRONMENTAL FACTORS AND IMMUNOLOGICAL DYSFUNCTION ROLE IN ENDOMETRIOSIS WILL BE SUMMARIZED. TO CONCLUDE, A LOT OF EFFORT MUST BE PUT TO INTEGRATE THE ABUNDANT DATA FROM GENETIC, EPIGENETIC AND IMMUNOLOGICAL STUDIES TO PROPOSE ONE COHERENT THEORY FOR THE PATHOGENESIS OF ENDOMETRIOSIS. 2017 4 1879 31 EMERGING ROLES OF NON-CODING RNAS IN PSORIASIS PATHOGENESIS. PSORIASIS IS A COMPLEX GENETIC SKIN DISORDER TYPICALLY MANIFESTED BY RED, SCALY, AND ITCHY PLAQUES MOST COMMONLY OVER THE SCALP, TRUNK, ELBOWS, AND KNEES. HISTOPATHOLOGICAL FEATURES INCLUDE THICKENING OF THE EPIDERMAL LAYER DUE TO HYPER-PROLIFERATION AND ABNORMAL DIFFERENTIATION OF EPIDERMAL KERATINOCYTES ALONG WITH INFILTRATION OF IMMUNE CELLS IN THE PSORIATIC SKIN. IT IS A CHRONIC INFLAMMATORY RELAPSING DISEASE, AND THERE IS CURRENTLY NO PERMANENT CURE FOR PSORIASIS. PROPER MEDICATIONS CAN REDUCE THE SEVERITY OF THE DISEASE AND IMPROVE THE QUALITY OF LIFE OF THE PATIENTS. WHILE THE GENETIC COMPONENTS OF PSORIASIS PATHOGENESIS ARE WELL EXPLORED, THE FULL UNDERSTANDING OF ITS EPIGENETIC COMPONENT REMAINS ELUSIVE. NON-CODING RNAS (NCRNAS) ARE DOCUMENTED TO REGULATE VARIOUS EPIGENETIC PROCESSES THAT LEAD TO THE PATHOGENESIS OF DIFFERENT DISEASES INCLUDING PSORIASIS. IN THIS REVIEW, WE HAVE DISCUSSED THE MOLECULAR INTERPLAY OF DIFFERENT NCRNAS IN PSORIASIS PATHOGENESIS. THE ROLES OF MICRORNAS (MIRNAS) IN PSORIASIS ARE PRETTY WELL STUDIED, WHEREAS THE ROLES OF LONG NONCODING RNAS (LNCRNAS) AND CIRCULAR RNAS (CIRCRNAS) ARE EMERGING. THIS REVIEW PROVIDES IDEAS COVERING SOME OF THE LATEST FINDINGS OF DIFFERENT MODES OF FUNCTIONS PLAYED BY THOSE DIFFERENT NCRNAS DOCUMENTED IN THE LITERATURE. AS AN EVER-EVOLVING TOPIC, SOME WORKS ARE STILL ONGOING AS WELL AS THERE ARE SEVERAL FIELDS THAT NEED RIGOROUS SCIENTIFIC VENTURES. WE HAVE PROPOSED THE AREAS WHICH CLAIM MORE EXPLORATIONS TO BETTER UNDERSTAND THE ROLES PLAYED BY THE NCRNAS IN PSORIASIS PATHOGENESIS. 2023 5 4720 28 NONCODING RNAS AS ADDITIONAL MEDIATORS OF EPIGENETIC REGULATION IN NONALCOHOLIC FATTY LIVER DISEASE. NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) HAS EMERGED AS THE MOST COMMON CAUSE OF CHRONIC LIVER DISORDER WORLDWIDE. IT REPRESENTS A SPECTRUM THAT INCLUDES A CONTINUUM OF DIFFERENT CLINICAL ENTITIES RANGING FROM SIMPLE STEATOSIS TO NONALCOHOLIC STEATOHEPATITIS, WHICH CAN EVOLVE TO CIRRHOSIS AND IN SOME CASES TO HEPATOCELLULAR CARCINOMA, ULTIMATELY LEADING TO LIVER FAILURE. THE PATHOGENESIS OF NAFLD AND THE MECHANISMS UNDERLYING ITS PROGRESSION TO MORE PATHOLOGICAL STAGES ARE NOT COMPLETELY UNDERSTOOD. BESIDES GENETIC FACTORS, EVIDENCE INDICATES THAT EPIGENETIC MECHANISMS OCCURRING IN RESPONSE TO ENVIRONMENTAL STIMULI ALSO CONTRIBUTE TO THE DISEASE RISK. NONCODING RNAS (NCRNAS), INCLUDING MICRORNAS, LONG NONCODING RNAS, AND CIRCULAR RNAS, ARE ONE OF THE EPIGENETIC FACTORS THAT PLAY KEY REGULATORY ROLES IN THE DEVELOPMENT OF NAFLD. AS THE FIELD OF NCRNAS IS RAPIDLY EVOLVING, THE PRESENT REVIEW AIMS TO EXPLORE THE CURRENT STATE OF KNOWLEDGE ON THE ROLES OF THESE RNA SPECIES IN THE PATHOGENESIS OF NAFLD, HIGHLIGHT RELEVANT MECHANISMS BY WHICH SOME NCRNAS CAN MODULATE REGULATORY NETWORKS IMPLICATED IN NAFLD, AND DISCUSS KEY CHALLENGES AND FUTURE DIRECTIONS FACING CURRENT RESEARCH IN THE HOPES OF DEVELOPING NCRNAS AS NEXT-GENERATION NON-INVASIVE DIAGNOSTICS AND THERAPIES IN NAFLD AND SUBSEQUENT PROGRESSION TO HEPATOCELLULAR CARCINOMA. 2022 6 4722 30 NONCODING RNAS IN NONALCOHOLIC FATTY LIVER DISEASE: POTENTIAL DIAGNOSIS AND PROGNOSIS BIOMARKERS. NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) IS CURRENTLY THE MOST COMMON CHRONIC LIVER DISEASE WORLDWIDE IN PART DUE TO THE CONCOMITANT OBESITY PANDEMIC AND INSULIN RESISTANCE (IR). IT IS INCREASINGLY BECOMING EVIDENT THAT NAFLD IS A DISEASE AFFECTING NUMEROUS EXTRAHEPATIC VITAL ORGANS AND REGULATORY PATHWAYS. THE MOLECULAR MECHANISMS UNDERLYING THE NONALCOHOLIC STEATOSIS FORMATION ARE POORLY UNDERSTOOD, AND LITTLE INFORMATION IS AVAILABLE ON THE PATHWAYS THAT ARE RESPONSIBLE FOR THE PROGRESSIVE HEPATOCELLULAR DAMAGE THAT FOLLOWS LIPID ACCUMULATION. RECENTLY, MUCH RESEARCH HAS FOCUSED ON THE IDENTIFICATION OF THE EPIGENETIC MODIFICATIONS THAT CONTRIBUTE TO NAFLD PATHOGENESIS. NONCODING RNAS (NCRNAS) ARE ONE OF SUCH EPIGENETIC FACTORS THAT COULD BE IMPLICATED IN THE NAFLD DEVELOPMENT AND PROGRESSION. IN THIS REVIEW, WE SUMMARIZE THE CURRENT KNOWLEDGE OF THE GENETIC AND EPIGENETIC FACTORS POTENTIALLY UNDERLYING THE DISEASE. PARTICULAR EMPHASIS WILL BE PUT ON THE CONTRIBUTION OF MICRORNAS (MIRNAS), LONG NONCODING RNAS (LNCRNAS), AND CIRCULAR RNAS (CIRCRNAS) TO THE PATHOPHYSIOLOGY OF NAFLD AS WELL AS THEIR POTENTIAL USE AS THERAPEUTIC TARGETS OR AS MARKERS FOR THE PREDICTION AND THE PROGRESSION OF THE DISEASE. 2020 7 6153 18 THE FUNCTION OF THE METALS IN REGULATING EPIGENETICS DURING PARKINSON'S DISEASE. PARKINSON'S MEANS PARKINSON'S DISEASE, A CHRONIC DEGENERATIVE DISEASE OF CENTRAL NERVOUS SYSTEM. THE MAIN AREA WHICH IS AFFECTED BY THIS DISEASE IS MOTOR SYSTEM. SINCE IT FIRSTLY FOUNDED BY JAMES PARKINSON IN HIS 1817 PUBLICATION, NOWADAYS, PEOPLE STILL HAVE LOTS OF QUESTIONS ABOUT THIS DISEASE. THIS REVIEW MAINLY SUMMARIZES THE EPIGENETICS OF PARKINSON'S. DNA METHYLATION IS ONE OF THE EPIGENETIC MECHANISMS OF PARKINSON'S. DURING THE DEVELOPMENT OF DISEASE, GLOBAL HYPOMETHYLATION, AND HYPERMETHYLATION HAPPEN IN DIFFERENT AREAS OF PATIENTS. ANOTHER EPIGENETIC MECHANISM IS HISTONE MODIFICATION. PEOPLE BELIEVE THAT SOME METALS CAN INDUCE PARKINSON'S DISEASE BY MODULATING EPIGENETIC MECHANISMS. THIS REVIEW SUMMARIZES THE RELATIONSHIPS BETWEEN DIFFERENT METALS AND PARKINSON'S DISEASE. HOWEVER, THE SPECIFIC ROLES OF MOST METALS IN EPIGENETICS ARE STILL UNKNOWN, WHICH NEED FURTHER RESEARCH. 2020 8 6784 15 [CHRONIC STRESS AND EPIGENETICS. RELATION BETWEEN ACADEMIC SCIENCES AND THEOLOGY]. THE AUTHOR GIVES A SHORT ACCOUNT ON THE PRINCIPLES OF SELYE'S STRESS THEORY, AND DISCUSSES SIMILARITIES AND DISSIMILARITIES OF ACUTE AND CHRONIC STRESS. BOTH THE EXTERNAL, AND THE INTERNAL ENVIRONMENT, AS WELL AS THE PSYCHO-MENTAL STATUS ARE INVOLVED IN THE NOTION OF THE ENVIRONMENT. BASIC PRINCIPLES OF EPIGENETICS ARE REVIEWED: INTERACTION BETWEEN ENVIRONMENT AND GENES, NEUROENDOCRINE AND ENZYMATIC MECHANISMS INVOLVED IN SILENCING AND ACTIVATION OF GENES, NOTIONS OF PHENOTYPIC PLASTICITY, AND EPIGENETIC REPROGRAMMING ARE DISCUSSED. EPIGENETIC MECHANISMS OF INTERRELATION BETWEEN PATHOLOGICAL CLINICAL STATES (DISEASES) AND THE CHARACTERISTIC PHENOTYPES, CAUSATIVE ROLE OF PSYCHO-MENTAL STATUS IN EVOKING PATHOLOGICAL SOMATIC ALTERATIONS, AND THE POTENTIAL THERAPEUTIC CONSEQUENCES ARE BRIEFLY DISCUSSED. THE ETIOLOGICAL ROLE OF CHRONIC, CIVILIZATION STRESS IN PRODUCING THE WORLDWIDE INCREMENT OF CARDIOVASCULAR MORBIDITY IS CITED, ARGUMENTATION AND CRITICISM OF THE CURRENT THERAPEUTICAL PRACTICE IS DISCUSSED. THE AUTHOR CONCLUDES THAT RECENT ADVANCES IN EPIGENETIC KNOWLEDGE SEEM TO SOLVE THE CONTROVERSY BETWEEN THE ACADEMIC AND THEOLOGICAL SCIENCES. 2012 9 5721 27 SIRTUINS-NOVEL REGULATORS OF EPIGENETIC ALTERATIONS IN AIRWAY INFLAMMATION. HISTONE MODIFICATION IS AN IMPORTANT EPIGENETIC ALTERATION, AND HISTONE DEACETYLASES ARE INVOLVED IN THE OCCURRENCE AND DEVELOPMENT OF VARIOUS RESPIRATORY DISEASES. SIRTUINS (SIRTS) HAVE BEEN DEMONSTRATED TO PLAY AN IMPORTANT ROLE IN THE FORMATION AND PROGRESSION OF CHRONIC INFLAMMATORY DISEASES OF THE RESPIRATORY TRACT. SIRTS PARTICIPATE IN THE REGULATION OF OXIDATIVE STRESS AND INFLAMMATION AND ARE RELATED TO CELL STRUCTURE AND CELLULAR LOCALIZATION. THIS PAPER SUMMARIZES THE ROLES AND MECHANISMS OF SIRTS IN AIRWAY INFLAMMATION AND DESCRIBES THE LATEST RESEARCH ON SIRT MODULATORS, AIMING TO PROVIDE A THEORETICAL BASIS FOR THE STUDY OF POTENTIAL EPIGENETIC ALTERATION-INDUCING DRUG TARGETS. 2022 10 1 14 ON DECEMBER 5, 2017, THE NATIONAL ACADEMIES OF SCIENCES, ENGINEERING, AND MEDICINE HOSTED A PUBLIC WORKSHOP TITLED NUTRIGENOMICS AND THE FUTURE OF NUTRITION IN WASHINGTON, DC, TO REVIEW CURRENT KNOWLEDGE IN THE FIELD OF NUTRIGENOMICS AS IT RELATES TO NUTRITION. WORKSHOP PARTICIPANTS EXPLORED THE INFLUENCE OF GENETIC AND EPIGENETIC EXPRESSION ON NUTRITIONAL STATUS AND THE POTENTIAL IMPACT OF PERSONALIZED NUTRITION ON HEALTH MAINTENANCE AND CHRONIC DISEASE PREVENTION. THIS PUBLICATION SUMMARIZES THE PRESENTATIONS AND DISCUSSIONS FROM THE WORKSHOP. 2018 11 757 32 CARTILAGE REPAIR BY MESENCHYMAL STEM CELLS: CLINICAL TRIAL UPDATE AND PERSPECTIVES. OSTEOARTHRITIS IS A DEGENERATIVE DISEASE OF JOINTS WITH DESTRUCTION OF ARTICULAR CARTILAGE ASSOCIATED WITH SUBCHONDRAL BONE HYPERTROPHY AND INFLAMMATION. OA IS THE LEADING CAUSE OF JOINT PAIN RESULTING IN SIGNIFICANT WORSENING OF THE QUALITY-OF-LIFE IN THE ELDERLY. NUMEROUS EFFORTS HAVE BEEN SPENT TO OVERCOME THE INHERENTLY POOR HEALING ABILITY OF ARTICULAR CARTILAGE. MESENCHYMAL STEM CELLS (MSCS) HAVE BEEN IN THE LIMELIGHT OF CELL-BASED THERAPIES TO PROMOTE CARTILAGE REPAIR. DESPITE PROGRESSIVE ADVANCEMENTS IN MSC MANIPULATION AND THE INTRODUCTION OF VARIOUS BIOACTIVE SCAFFOLDS AND GROWTH FACTORS IN PRECLINICAL STUDIES, CURRENT CLINICAL TRIALS ARE STILL AT EARLY STAGES WITH PRELIMINARY AIMS TO EVALUATE SAFETY, FEASIBILITY AND EFFICACY. THIS REVIEW SUMMARISES RECENTLY REPORTED MSC-BASED CLINICAL TRIALS AND DISCUSSES NEW RESEARCH DIRECTIONS WITH PARTICULAR FOCUS ON THE POTENTIAL APPLICATION OF MSC-DERIVED EXTRACELLULAR VEHICLES, MIRNAS AND ADVANCED GENE EDITING TECHNIQUES WHICH MAY SHED LIGHT ON THE DEVELOPMENT OF NOVEL TREATMENT STRATEGIES. THE TRANSLATIONAL POTENTIAL OF THIS ARTICLE: THIS REVIEW SUMMARISES RECENT MSC-RELATED CLINICAL RESEARCH THAT FOCUSES ON CARTILAGE REPAIR. WE ALSO PROPOSE A NOVEL POSSIBLE TRANSLATIONAL DIRECTION FOR HYALINE CARTILAGE FORMATION AND A NEW PARADIGM MAKING USE OF EXTRA-CELLULAR SIGNALLING AND EPIGENETIC REGULATION IN THE APPLICATION OF MSCS FOR CARTILAGE REPAIR. 2017 12 1243 21 CURRENT CONCEPTS IN CHRONIC INFLAMMATORY DISEASES: INTERACTIONS BETWEEN MICROBES, CELLULAR METABOLISM, AND INFLAMMATION. RECENT RESEARCH INDICATES THAT CHRONIC INFLAMMATORY DISEASES, INCLUDING ALLERGIES AND AUTOIMMUNE AND NEUROPSYCHIATRIC DISEASES, SHARE COMMON PATHWAYS OF CELLULAR AND MOLECULAR DYSREGULATION. IT WAS THE AIM OF THE INTERNATIONAL VON-BEHRING-RONTGEN SYMPOSIUM (OCTOBER 16-18, 2014, IN MARBURG, GERMANY) TO DISCUSS RECENT DEVELOPMENTS IN THIS FIELD. THESE INCLUDE A CONCEPT OF BIODIVERSITY; THE CONTRIBUTION OF URBANIZATION, LIFESTYLE FACTORS, AND NUTRITION (EG, VITAMIN D); AND NEW MECHANISMS OF METABOLIC AND IMMUNE DYSREGULATION, SUCH AS EXTRACELLULAR AND INTRACELLULAR RNAS AND CELLULAR AND MITOCHONDRIAL STRESS. EPIGENETIC MECHANISMS CONTRIBUTE FURTHER TO ALTERED GENE EXPRESSION AND THEREFORE TO THE DEVELOPMENT OF CHRONIC INFLAMMATION. THESE NOVEL FINDINGS PROVIDE THE FOUNDATION FOR FURTHER DEVELOPMENT OF PREVENTIVE AND THERAPEUTIC STRATEGIES. 2016 13 4844 26 ONE YEAR IN REVIEW 2019: PATHOGENESIS OF RHEUMATOID ARTHRITIS. RHEUMATOID ARTHRITIS (RA) IS A CHRONIC INFLAMMATORY AUTOIMMUNE DISEASE INFLUENCED BY BOTH GENETIC AND ENVIRONMENTAL FACTORS. OVER THE LAST FEW YEARS, PARTICULAR ATTENTION HAS BEEN GIVEN TO NOVEL GENES AND TO THE CLOSE INTERACTION BETWEEN GENETIC FACTORS AND EPIGENETIC MECHANISMS. RESEARCH HAS ALSO FOCUSED ON THE INFLUENCE OF ENVIRONMENTAL FACTORS ON DISEASE DEVELOPMENT, AND ON NEW MECHANISMS OF THE INNATE AND ADAPTIVE IMMUNE SYSTEM THAT CAN INFLUENCE THE DIFFERENT STAGES OF RA. HOWEVER, THERE ARE STILL SEVERAL ASPECTS OF THE DISEASE THAT NEED FURTHER INVESTIGATION. SHEDDING SOME LIGHT ON THE DIFFERENT ASPECTS OF RA PATHOGENESIS WILL HELP TO IMPROVE THE CURRENT DIAGNOSTIC TOOLS AND TO IDENTIFY NEW TARGETS FOR THE DEVELOPMENT OF DISEASE-MODIFYING THERAPIES. THUS, IN THIS REVIEW WE SUMMARISE THE NEW INSIGHTS IN RA PATHOGENESIS, RESULTING FROM LITERATURE RESEARCH DATA PUBLISHED IN THE LAST YEAR. 2019 14 3173 24 GUT MICROBIOTA-MICRORNA INTERACTIONS IN ANKYLOSING SPONDYLITIS. ANKYLOSING SPONDYLITIS (AS) IS A CHRONIC AUTOIMMUNE INFLAMMATORY DISABILITY THAT IS PART OF THE RHEUMATIC DISEASE GROUP OF SPONDYLOARTHROPATHIES. AS COMMONLY INFLUENCES THE JOINTS OF THE AXIAL SKELETON. THE CONTRIBUTIONS TO AS PATHOGENESIS OF GENETIC SUSCEPTIBILITY (PARTICULARLY HLA-B27 AND ERAP-1) AND EPIGENETIC MODIFICATIONS, LIKE NON-CODING RNAS, AS WELL AS ENVIRONMENTAL FACTORS, HAVE BEEN INVESTIGATED OVER THE LAST FEW YEARS. BUT THE FUNDAMENTAL ETIOLOGY OF AS REMAINS ELUSIVE TO DATE. THE EVIDENCE SUMMARIZED HERE INDICATES THAT IN THE IMMUNOPATHOGENESIS OF AS, MICRORNAS AND THE GUT MICROBIOME PERFORM CRITICAL FUNCTIONS. WE DISCUSS SIGNIFICANT ADVANCES IN THE IMMUNOLOGICAL MECHANISMS UNDERLYING AS AND ADDRESS POTENTIAL CROSS-TALK BETWEEN THE GUT MICROBIOME AND HOST MICRORNAS. THIS CRITICAL INTERACTION IMPLICATES A CO-EVOLUTIONARY SYMBIOTIC LINK BETWEEN HOST IMMUNITY AND THE GUT MICROBIOME. 2021 15 1867 28 EMERGING GENE-EDITING MODALITIES FOR OSTEOARTHRITIS. OSTEOARTHRITIS (OA) IS A PATHOLOGICAL DEGENERATIVE CONDITION OF THE JOINTS THAT IS WIDELY PREVALENT WORLDWIDE, RESULTING IN SIGNIFICANT PAIN, DISABILITY, AND IMPAIRED QUALITY OF LIFE. THE DIVERSE ETIOLOGY AND PATHOGENESIS OF OA CAN EXPLAIN THE PAUCITY OF VIABLE PREVENTIVE AND DISEASE-MODIFYING STRATEGIES TO COUNTER IT. ADVANCES IN GENOME-EDITING TECHNIQUES MAY IMPROVE DISEASE-MODIFYING SOLUTIONS BY ADDRESSING INHERITED PREDISPOSING RISK FACTORS AND THE ACTIVITY OF INFLAMMATORY MODULATORS. RECENT PROGRESS ON TECHNOLOGIES SUCH AS CRISPR/CAS9 AND CELL-BASED GENOME-EDITING THERAPIES TARGETING THE GENETIC AND EPIGENETIC ALTERNATIONS IN OA OFFER PROMISING AVENUES FOR EARLY DIAGNOSIS AND THE DEVELOPMENT OF PERSONALIZED THERAPIES. THE PURPOSE OF THIS LITERATURE REVIEW WAS TO CONCISELY SUMMARIZE THE GENOME-EDITING OPTIONS AGAINST CHRONIC DEGENERATIVE JOINT CONDITIONS SUCH AS OA WITH A FOCUS ON THE MORE RECENTLY EMERGING MODALITIES, ESPECIALLY CRISPR/CAS9. FUTURE ADVANCEMENTS IN NOVEL GENOME-EDITING THERAPIES MAY IMPROVE THE EFFICACY OF SUCH TARGETED TREATMENTS. 2020 16 6152 26 THE FUNCTION OF NCRNAS IN RHEUMATIC DISEASES. RHEUMATIC DISEASES ARE A GROUP OF CHRONIC HETEROGENEOUS AUTOIMMUNE DISORDERS CHARACTERIZED BY ABNORMAL REGULATION OF THE INNATE AND ADAPTIVE IMMUNE SYSTEMS. DESPITE EXTENSIVE EFFORTS, THE FULL SPECTRUM OF MOLECULAR FACTORS THAT CONTRIBUTE TO THE PATHOGENESIS OF RHEUMATIC DISEASES REMAINS UNCLEAR. NCRNAS CAN GOVERN GENE EXPRESSION AT THE TRANSCRIPTIONAL AND POST-TRANSCRIPTIONAL LEVELS IN MULTIPLE DISEASES. RECENT STUDIES HAVE DEMONSTRATED AN IMPORTANT ROLE FOR NCRNAS, SUCH AS MIRNAS AND LNCRNAS, IN THE DEVELOPMENT OF IMMUNE CELLS AND RHEUMATIC DISEASES. HERE, WE FOCUS ON THE EPIGENETIC REGULATORY ROLES OF NCRNAS IN THE PATHOGENESIS OF RHEUMATIC DISEASES AND AS BIOMARKERS OF DISEASE STATE. 2019 17 1233 27 CROSSTALK BETWEEN KIDNEY AND LIVER IN NON-ALCOHOLIC FATTY LIVER DISEASE: MECHANISMS AND THERAPEUTIC APPROACHES. LIVER AND KIDNEY ARE VITAL ORGANS THAT MAINTAIN HOMEOSTASIS AND INJURY TO EITHER OF THEM TRIGGERS PATHOGENIC PATHWAYS AFFECTING THE OTHER. FOR EXAMPLE, NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) PROMOTES THE PROGRESSION OF CHRONIC KIDNEY DISEASE (CKD), VICE VERSA ACUTE KIDNEY INJURY (AKI) ENDORSES THE INDUCTION AND PROGRESSION OF LIVER DYSFUNCTION. PROGRESS IN CLINICAL AND BASIC RESEARCH SUGGEST A ROLE OF EXCESSIVE FRUCTOSE INTAKE, INSULIN RESISTANCE, INFLAMMATORY CYTOKINES PRODUCTION, ACTIVATION OF THE RENIN-ANGIOTENSIN SYSTEM, REDOX IMBALANCE, AND THEIR IMPACT ON EPIGENETIC REGULATION OF GENE EXPRESSION IN THIS CONTEXT. RECENT DEVELOPMENTS IN EXPERIMENTAL AND CLINICAL RESEARCH HAVE IDENTIFIED SEVERAL BIOCHEMICAL AND MOLECULAR PATHWAYS FOR AKI-LIVER INTERACTION, INCLUDING ALTERED LIVER ENZYMES PROFILE, METABOLIC ACIDOSIS, OXIDATIVE STRESS, ACTIVATION OF INFLAMMATORY AND REGULATED CELL DEATH PATHWAYS. THIS REVIEW FOCUSES ON THE CURRENT PRECLINICAL AND CLINICAL FINDINGS ON KIDNEY-LIVER CROSSTALK IN NAFLD-CKD AND AKI-LIVER DYSFUNCTION SETTINGS AND HIGHLIGHTS POTENTIAL MOLECULAR MECHANISMS AND THERAPEUTIC TARGETS. 2022 18 4464 28 MOLECULAR MECHANISMS OF NONALCOHOLIC FATTY LIVER DISEASE (NAFLD)/NONALCOHOLIC STEATOHEPATITIS (NASH). NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) IS ONE OF THE MOST COMMON CHRONIC LIVER DISEASES WORLDWIDE AND HAS GARNERED INCREASING ATTENTION IN RECENT DECADES. NAFLD IS CHARACTERIZED BY A WIDE RANGE OF LIVER CHANGES, FROM SIMPLE STEATOSIS TO NONALCOHOLIC STEATOHEPATITIS (NASH), CIRRHOSIS, AND HEPATOCELLULAR CARCINOMA. THE PATHOGENESIS OF NAFLD/NASH IS VERY COMPLICATED AND INVOLVES LIPID ACCUMULATION, INSULIN RESISTANCE, INFLAMMATION, AND FIBROGENESIS. IN ADDITION, NAFLD IS CLOSELY ASSOCIATED WITH COMPLICATIONS SUCH AS OBESITY, DYSLIPIDEMIA, AND TYPE 2 DIABETES. IN PARTICULAR, THE CLINICAL SPECTRUM, PATHOPHYSIOLOGY, AND THERAPEUTIC OPTIONS OF NAFLD SHARE MANY THINGS IN COMMON WITH DIABETES. INSULIN RESISTANCE IS AN UNDERLYING BASIS FOR THE PATHOGENESIS OF DIABETES AND NAFLD. THIS CHAPTER FOCUSES ON THE MOLECULAR MECHANISM INVOLVED IN THE PATHOGENESIS OF INSULIN RESISTANCE, DIABETES, AND NASH/NAFLD INCLUDING THOSE THAT DRIVE DISEASE PROGRESSION SUCH AS OXIDATIVE STRESS, GENETIC AND EPIGENETIC MECHANISMS, ADIPONECTIN, CYTOKINES, AND IMMUNE CELLS. 2021 19 2224 27 EPIGENETIC MODIFICATIONS IN THE PATHOGENESIS OF SYSTEMIC SCLEROSIS. SYSTEMIC SCLEROSIS IS A RARE CHRONIC AUTOIMMUNE DISEASE, WHICH MAINLY MANIFESTS AS IMMUNE DISORDERS, VASCULAR DAMAGE, AND PROGRESSIVE FIBROSIS. THE ETIOLOGY OF SSC IS COMPLEX AND INVOLVES MULTIPLE FACTORS. BOTH GENETIC AND ENVIRONMENTAL FACTORS ARE INVOLVED IN ITS PATHOGENESIS. AS ONE OF THE MOLECULAR MECHANISMS OF ENVIRONMENTAL FACTORS, EPIGENETIC REGULATION PLAYS AN IMPORTANT ROLE IN THE OCCURRENCE AND DEVELOPMENT OF SYSTEMIC SCLEROSIS, WHICH INVOLVES DNA METHYLATION, HISTONE MODIFICATION AND NON-CODING RNA REGULATION. THIS REVIEW SUMMARIZES RESEARCH ADVANCES IN EPIGENETICS, INCLUDING EXOSOMES, LNCRNA, AND MENTIONS POSSIBLE BIOMARKERS AND THERAPEUTIC TARGETS AMONG THEM. 2022 20 5300 26 PROTEIN METHYLATION IN DIABETIC KIDNEY DISEASE. CHRONIC KIDNEY DISEASE (CKD) IS DEFINED BY PERSISTENT URINE ABERRATIONS, STRUCTURAL ABNORMALITIES, OR IMPAIRED EXCRETORY RENAL FUNCTION. DIABETES IS THE LEADING CAUSE OF CKD. THEIR COMMON PATHOLOGICAL MANIFESTATION IS RENAL FIBROSIS. APPROXIMATELY HALF OF ALL PATIENTS WITH TYPE 2 DIABETES AND ONE-THIRD WITH TYPE 1 DIABETES WILL DEVELOP CKD. HOWEVER, RENAL FIBROSIS MECHANISMS ARE STILL POORLY UNDERSTOOD, ESPECIALLY POST-TRANSCRIPTIONAL AND EPIGENETIC REGULATION. AND AN UNMET NEED REMAINS FOR INNOVATIVE TREATMENT STRATEGIES FOR PREVENTING, ARRESTING, TREATING, AND REVERSING DIABETIC KIDNEY DISEASE (DKD). PEOPLE BELIEVE THAT PROTEIN METHYLATION, INCLUDING HISTONE AND NON-HISTONE, IS AN ESSENTIAL TYPE OF POST-TRANSLATIONAL MODIFICATION (PTM). HOWEVER, PREVALENT REVIEWS MAINLY FOCUS ON THE CAUSES SUCH AS DNA METHYLATION. THIS REVIEW WILL TAKE INSIGHTS INTO THE PROTEIN PART. FURTHERMORE, BY EMPHASIZING THE CLOSE RELATIONSHIP BETWEEN PROTEIN METHYLATION AND DKD, WE WILL SUMMARIZE THE CLINICAL RESEARCH STATUS AND FORESEE THE APPLICATION PROSPECT OF PROTEIN METHYLTRANSFERASE (PMT) INHIBITORS IN DKD TREATMENT. IN A NUTSHELL, OUR REVIEW WILL CONTRIBUTE TO A MORE PROFOUND UNDERSTANDING OF DKD'S MOLECULAR MECHANISM AND INSPIRE PEOPLE TO DIG INTO THIS FIELD. 2022