Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly oxygen-consuming organs that are sensitive to mitochondrial dysfunction. Moreover, the fibrotic process of skin and islet is closely related to mitochondrial dysfunction as well. This review summarized emerging mechanisms related to mitochondrial dysfunction in different fibrotic organs and tissues above. First, it highlighted the important elucidation of mitochondria morphological changes, mitochondrial membrane potential and structural damage, mitochondrial DNA (mtDNA) damage and reactive oxidative species (ROS) production, etc. Second, it introduced the abnormality of mitophagy and mitochondrial transfer also contributed to the fibrotic process. Therefore, with gaining the increasing knowledge of mitochondrial structure, function, and origin, we could kindle a new era for the diagnostic and therapeutic strategies of many fibrotic diseases based on mitochondrial dysfunction.

In mid-December 2019, a novel atypical pneumonia broke out in Wuhan, Hubei Province, China and was caused by a newly identified coronavirus, initially termed 2019 Novel Coronavirus and subsequently severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As of 19 May 2020, a total of 4,731,458 individuals were reported as infected with SARS-CoV-2 among 213 countries, areas or territories with recorded cases, and the overall case-fatality rate was 6.6% (316,169 deaths among 4,731,458 recorded cases), according to the World Health Organization. Studies have shown that SARS-CoV-2 is notably similar to (severe acute respiratory syndrome coronavirus) SARS-CoV that emerged in 2002–2003 and Middle East respiratory syndrome coronavirus (MERS-CoV) that spread during 2012, and these viruses all contributed to global pandemics. The ability of SARS-CoV-2 to rapidly spread a pneumonia-like disease from Hubei Province, China, throughout the world has provoked widespread concern. The main symptoms of coronavirus disease 2019 (COVID-19) include fever, cough, myalgia, fatigue and lower respiratory signs. At present, nucleic acid tests are widely recommended as the optimal method for detecting SARS-CoV-2. However, obstacles remain, including the global shortage of testing kits and the presentation of false negatives. Experts suggest that almost everyone in China is susceptible to SARS-CoV-2 infection, and to date, there are no effective treatments. In light of the references published, this review demonstrates the biological features, spread, diagnosis and treatment of SARS-CoV-2 as a whole and aims to analyse the similarities and differences among SARS-CoV-2, SARS-CoV and MERS-CoV to provide new ideas and suggestions for prevention, diagnosis and clinical treatment.

Sepsis is a systemic inflammatory response syndrome caused by infection. With high morbidity and mortality of this disease, there is a need to find early effective diagnosis and assessment methods to improve the prognosis of patients. Heparin-binding protein (HBP) is a granular protein derived from polynuclear neutrophils. The biosynthetic HBP in neutrophils is rapidly released under the stimulation of bacteria, resulting in increased vascular permeability and edema. It is reasonable to speculate that the HBP in plasma may serve as a novel diagnostic marker for sepsis, bacterial skin infection, acute bacterial meningitis, leptospirosis, protozoan parasites, and even some noncommunicable diseases. It implies that in the detection and diagnosis of sepsis, it will be possible to make relevant diagnosis through this new indicator in the future. In this review, we summarize the typical biological function of HBP and its latest research progress to provide theoretical basis for clinical prediction and diagnosis of sepsis.

Tribbles homolog 3 (TRIB3) mediating signaling pathways are closely related to blood pressure regulation. Our previous findings suggested a greater benefit on vascular outcomes in patients carrying TRIB3 (251, A > G, rs2295490) G allele with good glucose and blood pressure control. And TRIB3 (rs2295490) AG/GG genotypes were found to reduce primary vascular events in type 2 diabetic patients who received intensive glucose treatment as compared to those receiving standard glucose treatment. However, the effect of TRIB3 genetic variation on antihypertensives was not clear in essential hypertension patients. A total of 368 patients treated with conventional dosage of antihypertensives (6 groups, grouped by atenolol/bisoprolol, celiprolol, doxazosin, azelnidipine/nitrendipine, imidapril, and candesartan/irbesartan) were enrolled in our study. Genetic variations were successfully identified by sanger sequencing. A linear mixed model analysis was performed to evaluate blood pressures among TRIB3 (251, A > G) genotypes and adjusted for baseline age, gender, body mass index, systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol and other biochemical factors appropriately. Our data suggested that TRIB3 (251, A > G) AA genotype carriers showed better antihypertensive effect than the AG/GG genotype carriers [P = 0.014 for DBP and P = 0.042 for mean arterial pressure (MAP)], with a maximal reduction of DBP by 4.2 mmHg and MAP by 3.56 mmHg after azelnidipine or nitrendipine treatment at the 4th week. Similar tendency of DBP-change and MAP-change was found for imidapril (ACEI) treatment, in which marginally significances were achieved (P = 0.073 and 0.075, respectively). Against that, we found that TRIB3 (251, A > G) AG/GG genotype carriers benefited from antihypertensive therapy of ARBs with a larger DBP-change during the period of observation (P = 0.036). Additionally, stratified analysis revealed an obvious difference of the maximal blood pressure change (13 mmHg for the MAP between male and female patients with AA genotype who took ARBs). Although no significant difference in antihypertensive effect between TRIB3 (251, A > G) genotypes in patients treated with α, β-ADRs was observed, we found significant difference in age-, sex-dependent manner related to α, β-ADRs. In conclusion, our data supported that TRIB3 (251, A > G) genetic polymorphism may serve as a useful biomarker in the treatment of hypertension.

China has achieved certain progress in expanding the coverage of primary healthcare institutions (PHCI), promoting equitable access to essential medical and health resources, and advancing universal health coverage. However, disparities in equitable access among different regions and income groups remain substantial. This study aims to analyze regional differences in the distribution of PHCI after the new healthcare reform and to explore the main factors influencing their distribution, so as to provide references for optimizing the allocation of primary healthcare resources. Data on the number of PHCI and factors influencing regional distribution differences from 2009 to 2022 were collected for 31 provincial-level administrative regions (hereinafter referred to as "administrative regions"). The Gini coefficient, Theil index, and the PHCI health resources density index (PHRDI) were used to evaluate the equity of PHCI distribution from 2009 to 2022 based on population, geographic area, and health level. PHRDI and each influencing factor were classified into 5 levels using the natural breaks method, and statistical maps of annual PHRDI distribution for each administrative region were drawn accordingly. Taking the number of PHCI in 2022 as the dependent variable, 15 indicators were selected as independent variables, and a geodetector was used to analyze the key factors influencing PHCI distribution. In 2022, the number of PHCI in China was 979 768, representing an increase of 11.07% compared with 2009. The distribution of PHCI in 2022 by year-end permanent resident population (Gini coefficient 0.178, Theil index 0.051) was absolutely equitable; distribution by the number of women receiving systematic maternal management (Gini coefficient 0.227, Theil index 0.084)/the number of low-birth-weight infants (Gini coefficient 0.335, Theil index 0.179) was relatively even/comparatively appropriate; distribution by geographic area (Gini coefficient 0.628, Theil index 0.701) was highly inequitable, with inter-regional and intra-regional differences contributing 58.45% and 41.55%, respectively, to the overall inequity by geographic area. Over the years, PHRDI consistently showed a gradual decline from eastern to western regions. Compared with 2009, 10 administrative regions achieved an upgrade in PHRDI level by 2022, with the largest number in the eastern region (5 administrative regions). Year-end permanent resident population, number of PHCI health personnel, number of women receiving systematic maternal management, geographic area, local health expenditure, regional GDP, and total dependency ratio were the main factors influencing regional differences in PHCI distribution (all P<0.05). The individual explanatory powers of these indicators were 75.6%, 69.3%, 68.0%, 47.3%, 44.9%, 44.0%, and 41.5%, respectively, and there were enhanced interaction effects among the influencing factors. The total number of PHCI in China has increased, but the growth rate is relatively slow and human resources remain relatively insufficient. There are regional differences in PHCI distribution, with PHRDI showing a gradual decrease from east to west. The establishment of PHCI should not only consider regional population size, but also comprehensively take into account factors such as local health personnel, economic development, health level, age structure, and geographic area.