Chronic liver disease or repeated damage to hepatocytes can give rise to hepatic fibrosis. Hepatic fibrosis (HF) is a pathological process of excessive sedimentation of extracellular matrix (ECM) proteins such as collagens, glycoproteins, and proteoglycans (PGs) in the hepatic parenchyma. Changes in the composition of the ECM lead to the stiffness of the matrix that destroys its inherent mechanical homeostasis, and a mechanical homeostasis imbalance activates hepatic stellate cells (HSCs) into myofibroblasts, which can overproliferate and secrete large amounts of ECM proteins. Excessive ECM proteins are gradually deposited in the Disse gap, and matrix regeneration fails, which further leads to changes in ECM components and an increase in stiffness, forming a vicious cycle. These processes promote the occurrence and development of hepatic fibrosis. In this review, the dynamic process of ECM remodeling of HF and the activation of HSCs into mechanotransduction signaling pathways for myofibroblasts to participate in HF are discussed. These mechanotransduction signaling pathways may have potential therapeutic targets for repairing or reversing fibrosis.

The purpose of this study was to screen for changes in chemokine and chemokine‐related genes that are expressed in hepatocellular carcinoma (HCC) as potential markers of HCC progression. Total RNA was extracted from tumor and peritumor tissues from mice with HCC and analyzed using a PCR microarray comprising 98 genes. Changes in gene expression of threefold or more were screened and subsequently confirmed by immunohistochemical analyses and western blotting. Furthermore, whether chemokine knockdown by RNA interference (RNAi) could significantly suppress tumor growth in vivo was also evaluated. Finally, total serum samples were collected from HCC patients with HBV/cirrhosis (n = 16) or liver cirrhosis (n = 16) and from healthy controls (n = 16). The serum mRNA and protein expression levels of CXCL1 in primary liver cancer patients were detected by qRT‐PCR and western blot analysis, respectively. Several genes were up‐regulated in tumor tissues during the progression period, including CXCL1, CXCL2, CXCL3, and IL‐1β, while CXCR1 expression was down‐regulated. CBRH‐7919 cells carrying CXCL1 siRNA resulted in decreased tumor growth in nude mice. The differences in serum CXCL1 mRNA and protein levels among the HCC, hepatic sclerosis (HS), and control groups were significant (P < 0.001). The mRNA and protein levels of CXCL1 in the HCC group were up‐regulated compared with the HS group or the control group (P < 0.001). Several chemokine genes were identified that might play important roles in the tumor microenvironment of HCC. These results provide new insights into human HCC and may ultimately facilitate early HCC diagnosis and lead to the discovery of innovative therapeutic approaches for HCC.

Despite widely reported fluorescence sensors for cations, direct detection of anions is nevertheless still rare. In this work, ionic liquid-functionalized fluorescent carbon nanoribbons (IL-CNRs) are one-step synthesized and serve as the fluorescent probes for direct and sensitive detection of sulfide ions (S²⁻). The IL-CNRs are synthesized based on electrochemical exfoliation of graphite rods in a water-IL biphasic system. The as-prepared IL-CNRs exhibit uniform structure, high crystallinity, strong blue fluorescence (absolute photoluminescence quantum yield of 11.4%), and unique selectivity towards S²⁻. Based on the fluorescence quenching of IL-CNRs by S²⁻, a fluorescence sensor is developed for direct, rapid and sensitive detection of S²⁻ in the range of 100 nM to 1 μM and 1–300 μM with a low detection limit (LOD, 85 nM). Moreover, detection of S²⁻ in a real sample (tap water) is also demonstrated.